Air pollution tied to survival odds for liver cancer patients

Air pollution tied to survival odds for liver cancer patients

By Madeline Kennedy

(Reuters Health) – For people diagnosed with liver cancer, living in an area with heavy air pollution from industry, traffic or smoke is linked to lower odds of survival, a California study finds.

The association between levels of tiny particles known as PM 2.5 in the air and death from liver cancer or from any cause was strongest for people with the least advanced cancers, researchers report in the International Journal of Cancer.

“Our study suggests that liver cancer patients may be another susceptible group that could benefit from reductions in air pollution,” study co-author Sandrah Eckel of the University of Southern California in Los Angeles said by email.

The liver may be at a high risk because it is responsible for helping the body process toxic materials that enter from the outside, she added.

PM 2.5 pollution is made up of small particles and droplets less than 2.5 microns in diameter. These particles, which are tiny enough to enter the bloodstream through the lungs, are usually the product of combustion – including smoke and fumes from industrial sources and power plants, vehicle engines, wildfires or indoor cooking fires.

Air pollution has been shown to increase lung cancer risk, but it may affect other cancers as well, the study team writes.

The U.S. has standards to control air pollution, but some areas like Los Angeles still go above the allowed levels, Eckel noted. Globally, air pollution may be as much as 10 times the U.S. standard, she said.

To see if there is a link between air pollution and liver cancer survival, the researchers used data on over 20,000 patients with the most common form of liver cancer, hepatocellular carcinoma.

The researchers included all patients who were diagnosed between 2000 and 2009 and listed in the California Cancer Registry.

The research team also used air pollution measurements from the areas where patients lived based on data from the Environmental Protection Agency’s Air Quality System database.

They found that people who were exposed to higher levels of PM 2.5 pollution after being diagnosed were significantly more likely to die from liver cancer or any cause.

For people with localized liver cancer, higher levels of pollution exposure were tied to a 31 percent higher risk of death from any cause compared to people with the same stage cancer exposed to the least pollution. For those whose cancer had spread to nearby tissues, the increased risk associated with higher pollution exposure was 5 percent and for those whose cancer had spread further in their body, the added risk was 10 percent.

The risk differences were similar for death from liver cancer, the researchers note.

Researchers adjusted for factors that might influence the analysis, like the patients’ socioeconomic status, distance from the pollution monitoring station and the size of the city they lived in.

A strength of the study is having included all liver cancer patients in the state registry for a good representation of this population, the authors note. One limitation is that researchers didn’t have much information about patients’ personal details and behaviors, like weight, alcohol consumption and whether they had hepatitis A or B.

“There is increasing evidence that particulate air pollutants can lead to early death from cardiorespiratory disease as well as a range of cancers including liver cancer,” Neil Thomas of the University of Birmingham in the UK said by email.

People can try to reduce their exposure by using air filters, wearing masks and avoiding indoor pollution like burning candles, but the most important step is to put pressure on lawmakers to improve air quality, said Thomas, who was not involved in the study.

“Air pollution reduction should be the goal of everyone for their own health and that of future generations,” Thomas said.

“We generally recommend that people monitor their local air quality index,” said Eckel, noting that in the U.S., local data from the EPA’s air quality monitoring system can be found on the website. “On high pollution days, you might want to stay indoors, close the windows, and clean the air indoors using filters,” Eckel said, and drivers should roll up their windows on busy roads.

SOURCE: International Journal of Cancer, online June 7, 2017

7 million premature deaths annually linked to air pollution – 2012

7 million premature deaths annually linked to air pollution – 2012

In new estimates released today, WHO reports that in 2012 around 7 million people died – one in eight of total global deaths – as a result of air pollution exposure. This finding more than doubles previous estimates and confirms that air pollution is now the world’s largest single environmental health risk. Reducing air pollution could save millions of lives.

New estimates

In particular, the new data reveal a stronger link between both indoor and outdoor air pollution exposure and cardiovascular diseases, such as strokes and ischaemic heart disease, as well as between air pollution and cancer. This is in addition to air pollution’s role in the development of respiratory diseases, including acute respiratory infections and chronic obstructive pulmonary diseases.

The new estimates are not only based on more knowledge about the diseases caused by air pollution, but also upon better assessment of human exposure to air pollutants through the use of improved measurements and technology. This has enabled scientists to make a more detailed analysis of health risks from a wider demographic spread that now includes rural as well as urban areas.

Regionally, low- and middle-income countries in the WHO South-East Asia and Western Pacific Regions had the largest air pollution-related burden in 2012, with a total of 3.3 million deaths linked to indoor air pollution and 2.6 million deaths related to outdoor air pollution.

“Cleaning up the air we breathe prevents non-communicable diseases as well as reduces disease risks among women and vulnerable groups, including children and the elderly…”

Dr Flavia Bustreo, WHO Assistant Director-General Family, Women and Children’s Health

“Cleaning up the air we breathe prevents noncommunicable diseases as well as reduces disease risks among women and vulnerable groups, including children and the elderly,” says Dr Flavia Bustreo, WHO Assistant Director-General Family, Women and Children’s Health. “Poor women and children pay a heavy price from indoor air pollution since they spend more time at home breathing in smoke and soot from leaky coal and wood cook stoves.”

Included in the assessment is a breakdown of deaths attributed to specific diseases, underlining that the vast majority of air pollution deaths are due to cardiovascular diseases as follows:

Outdoor air pollution-caused deaths – breakdown by disease:

  • 40% – ischaemic heart disease;
  • 40% – stroke;
  • 11% – chronic obstructive pulmonary disease (COPD);
  • 6% – lung cancer; and
  • 3% – acute lower respiratory infections in children.

Indoor air pollution-caused deaths – breakdown by disease:

  • 34% – stroke;
  • 26% – ischaemic heart disease;
  • 22% – COPD;
  • 12% – acute lower respiratory infections in children; and
  • 6% – lung cancer.

The new estimates are based on the latest WHO mortality data from 2012 as well as evidence of health risks from air pollution exposures. Estimates of people’s exposure to outdoor air pollution in different parts of the world were formulated through a new global data mapping. This incorporated satellite data, ground-level monitoring measurements and data on pollution emissions from key sources, as well as modelling of how pollution drifts in the air.

Risks factors are greater than expected

“The risks from air pollution are now far greater than previously thought or understood, particularly for heart disease and strokes,” says Dr Maria Neira, Director of WHO’s Department for Public Health, Environmental and Social Determinants of Health. “Few risks have a greater impact on global health today than air pollution; the evidence signals the need for concerted action to clean up the air we all breathe.”

After analysing the risk factors and taking into account revisions in methodology, WHO estimates indoor air pollution was linked to 4.3 million deaths in 2012 in households cooking over coal, wood and biomass stoves. The new estimate is explained by better information about pollution exposures among the estimated 2.9 billion people living in homes using wood, coal or dung as their primary cooking fuel, as well as evidence about air pollution’s role in the development of cardiovascular and respiratory diseases, and cancers.

In the case of outdoor air pollution, WHO estimates there were 3.7 million deaths in 2012 from urban and rural sources worldwide.

Many people are exposed to both indoor and outdoor air pollution. Due to this overlap, mortality attributed to the two sources cannot simply be added together, hence the total estimate of around 7 million deaths in 2012.

“Excessive air pollution is often a by-product of unsustainable policies in sectors such as transport, energy, waste management and industry. In most cases, healthier strategies will also be more economical in the long term due to health-care cost savings as well as climate gains,” says Dr Carlos Dora, WHO Coordinator for Public Health, Environmental and Social Determinants of Health. “WHO and health sectors have a unique role in translating scientific evidence on air pollution into policies that can deliver impact and improvements that will save lives.”

The release of today’s data is a significant step in advancing a WHO roadmap for preventing diseases related to air pollution. This involves the development of a WHO-hosted global platform on air quality and health to generate better data on air pollution-related diseases and strengthened support to countries and cities through guidance, information and evidence about health gains from key interventions.

Later this year, WHO will release indoor air quality guidelines on household fuel combustion, as well as country data on outdoor and indoor air pollution exposures and related mortality, plus an update of air quality measurements in 1600 cities from all regions of the world.

For more information, contact

Mr Tarik Jasarevic
Mobile: +41 79 367 6214
Telephone: +41 22 791 5099

Glenn Thomas
Telephone: +41 22 791 3983
Mobile: +41 79 509 0677

Outdoor Air Pollution

Key facts

  • Air pollution is a major environmental risk to health. By reducing air pollution levels, countries can reduce the burden of disease from stroke, heart disease, lung cancer, and both chronic and acute respiratory diseases, including asthma.
  • The lower the levels of air pollution, the better the cardiovascular and respiratory health of the population will be, both long- and short-term.
  • The “WHO Air quality guidelines” provide an assessment of health effects of air pollution and thresholds for health-harmful pollution levels.
  • In 2014, 92% of the world population was living in places where the WHO air quality guidelines levels were not met.
  • Ambient (outdoor air pollution) in both cities and rural areas was estimated to cause 3 million premature deaths worldwide in 2012.
  • Some 88% of those premature deaths occurred in low- and middle-income countries, and the greatest number in the WHO Western Pacific and South-East Asia regions.
  • Policies and investments supporting cleaner transport, energy-efficient housing, power generation, industry and better municipal waste management would reduce key sources of urban outdoor air pollution.
  • Reducing outdoor emissions from household coal and biomass energy systems, agricultural waste incineration, forest fires and certain agro-forestry activities (e.g. charcoal production) would reduce key rural and peri-urban air pollution sources in developing regions.
  • Reducing outdoor air pollution also reduces emissions of CO2 and short-lived climate pollutants such as black carbon particles and methane, thus contributing to the near- and long-term mitigation of climate change.
  • In addition to outdoor air pollution, indoor smoke is a serious health risk for some 3 billion people who cook and heat their homes with biomass fuels and coal.

Exposure to air pollution and Alzheimer’s development

Summary: Study raises further concern about exposure to air pollution and Alzheimer’s development.

Source: IOS Press.

Combustion-derived nanoparticles in key brain target cells and organelles in young urbanites.

A new study by researchers at the University of Montana, Universidad del Valle de México, Instituto Nacional de Pediatría, Boise State, and Universidad Nacional Autónoma de México, heightens concerns over the detrimental short- and long-term impact of airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) present in young urbanites’ brains. Using transmission electron microscopy, the researchers documented by abundant combustion nanoparticles in neurons, glial cells, choroid plexus, and neurovascular units of Mexico City children, teens and young adults chronically exposed to concentrations above the US-EPA standards for fine particulate matter. Residents in Mexico City are exposed from conception to harmful neurotoxic air pollutants. These findings are published in the Journal of Alzheimer’s Disease.

The detrimental impact of these tiny particles getting into the brain through the nasal and olfactory epithelium, the lungs and the gastrointestinal system is quickly recognized by extensive alterations in critical neuronal organelles including mitochondria, as well as axons and dendrites. Since these nanoparticles are in close contact with neurofilaments, glial fibers and chromatin, the researchers are very concerned about their potential for altering microtubule dynamics, accumulation and aggregation of unfolded proteins, mitochondrial dysfunction, altered calcium homeostasis and insulin signaling, and epigenetic changes.

Mexico City children, teens and young adults have shown key markers of Alzheimer’s disease (AD): hyperphosphorylated tau and amyloid plaques along with significant brain and intrathecal neuroinflammation, dysregulated immune responses, breakdown of epithelial and endothelial barriers, extensive damage to the neurovascular unit, and brain accumulation of metals associated with combustion. Moreover, these seemingly healthy young people have olfaction deficits, dysregulation of feeding hormones, deficiencies in attention and short-term memory, and below-average scores in Verbal and Full Scale IQ compared to age, gender, and socioeconomic status-matched low air pollution residents. The cognitive problem is particularly serious for overweight female teens carrying an allele of the apolipoprotein E (APOE) ε4, the most prevalent genetic risk factor for AD.

“In the context of serious continuous exposures to high concentrations of fine particulate matter (PM 2.5) and ozone, our current electron microscopy findings and the extensive literature associating air pollutants with brain damage, the issue of who is at risk of neurodegeneration at an early age should be an urgent public health concern,” said Dr. Lilian Calderon-Garcidueňas. “The effects of poverty, urban violence and urban stress on impaired cognitive skills are also very important for the developing brain and can’t be ignored. We know gender, BMI, and APOE influence children’s cognitive responses to air pollution.”

According to the researchers, the problem of having combustion-derived nanoparticles in children’s brains — developing brains — is very serious. These particles are ubiquitous and present in high concentrations in children as young as 3 years old. The particles contain transition neurotoxic metals and they are certainly causing extensive brain damage in key organelles. “The predominant combustion particles in young brains have properties that enable them to cause oxidative damage because these nanoparticles are capable of crossing all barriers. No barrier is spared,” Dr. Calderón-Garcidueňas emphasized.

Angélica González-Maciel added, “People with children and teens struggling in school and facing a significant increase of violence in school, streets, parks, and public transportation are deeply concerned about the impact these particles have on children’s behavioral patterns and academic performance and parents question what they can do to protect their families”.

All involved researchers agreed that in spite of the driving restrictions policies [that are clearly ineffective (Davis LW. Sci Rep 7: 41652, 2017)], millions of Mexico City residents continue to be exposed to very unhealthy concentrations of both PM 2.5 and ozone, both known risk factors for AD.

“Our results,” said Dr. Calderón-Garcidueňas, “highlight the urgent need for significantly decreasing the concentrations of fine particulate matter and ozone in Mexico City and the adjacent polluted states. Multidisciplinary intervention strategies could provide paths for prevention or amelioration of air pollution targeted cognitive deficits and possible long-term AD progression.”

Image shows brain slices.

The combined effects of combustion-derived nanoparticles, residency in a highly-polluted city, poor nutrition, obesity, metabolic syndrome, urban stress, lower brain and cognitive reserves, and APOE ε4 could lead to an acceleration of neurodegenerative changes among precarious young brains.

The authors concluded: highly oxidative, combustion nanoparticles entering young developing brains — the culprit hidden in plain sight in Alzheimer’s disease development — constitute a very serious public health issue, with grave social and economic consequences.

Efforts should also be aimed to identify and neuroprotect high risk young populations. Unfortunately, to date that is not happening.


Source: Lilian Calderon-Garcidueňas – IOS Press
Image Source: image is credited to Dr. Lilian Calderone.
Original Research: Abstract for “Apolipoprotein E4, Gender, Body Mass Index, Inflammation, Insulin Resistance, and Air Pollution Interactions: Recipe for Alzheimer’s Disease Development in Mexico City Young Females” by Calderón-Garcidueñas, Lilian and de la Monte, Suzanne M. in Journal of Alzheimer’s Disease. Published online July 8 2017 doi:10.3233/JAD-161299

IOS Press “Culprit Hidden in Plain Sight in Alzheimer’s Development.” NeuroscienceNews. NeuroscienceNews, 8 June 2017.


Apolipoprotein E4, Gender, Body Mass Index, Inflammation, Insulin Resistance, and Air Pollution Interactions: Recipe for Alzheimer’s Disease Development in Mexico City Young Females

Given the epidemiological trends of increasing Alzheimer’s disease (AD) and growing evidence that exposure and lifestyle factors contribute to AD risk and pathogenesis, attention should be paid to variables such as air pollution, in order to reduce rates of cognitive decline and dementia. Exposure to fine particulate matter (PM2.5) and ozone (O3) above the US EPA standards is associated with AD risk. Mexico City children experienced pre- and postnatal high exposures to PM2.5, O3, combustion-derived iron-rich nanoparticles, metals, polycyclic aromatic hydrocarbons, and endotoxins. Exposures are associated with early brain gene imbalance in oxidative stress, inflammation, innate and adaptive immune responses, along with epigenetic changes, accumulation of misfolded proteins, cognitive deficits, and brain structural and metabolic changes. The Apolipoprotein E (APOE) 4 allele, the most prevalent genetic risk for AD, plays a key role in the response to air pollution in young girls. APOE 4 heterozygous females with >75% to <94% BMI percentiles are at the highest risk of severe cognitive deficits (1.5–2 SD from average IQ). This review focused on the relationships between gender, BMI, systemic and neural inflammation, insulin resistance, hyperleptinemia, dyslipidemia, vascular risk factors, and central nervous system involvement in APOE4 urbanites exposed to PM2.5 and magnetite combustion-derived iron-rich nanoparticles that can reach the brain. APOE4 young female heterozygous carriers constitute a high-risk group for a fatal disease: AD. Multidisciplinary intervention strategies could be critical for prevention or amelioration of cognitive deficits and long-term AD progression in young individuals at high risk.

“Apolipoprotein E4, Gender, Body Mass Index, Inflammation, Insulin Resistance, and Air Pollution Interactions: Recipe for Alzheimer’s Disease Development in Mexico City Young Females” by Calderón-Garcidueñas, Lilian and de la Monte, Suzanne M. in Journal of Alzheimer’s Disease. Published online July 8 2017 doi:10.3233/JAD-161299

Climate Change , the facts

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GREENHOUSE GASES such as carbon dioxide (CO2) absorb heat (infrared radiation) emitted from Earth’s surface. Increases in the atmospheric concentrations of these gases cause Earth to warm by trapping more of this heat. Human activities—especially the burning of fossil fuels since the start of the Industrial Revolution—have increased atmospheric CO2 concentrations by about 40%, with more than half the increase occurring since 1970. Since 1900, the global average surface temperature has increased by about 0.8 °C (1.4 °F). This has been accompanied by warming of the ocean, a rise in sea level, a strong decline in Arctic sea ice, and many other associated climate effects. Much of this warming has occurred in the last four decades.

Detailed analyses have shown that the warming during this period is mainly a result of the increased concentrations of CO2 and other greenhouse gases. Continued emissions of these gases will cause further climate change, including substantial increases in global average surface temperature and important changes in regional climate. The magnitude and timing of these changes will depend on many factors, and slowdowns and accelerations in warming lasting a decade or more will continue to occur. However, long-term climate change over many decades will depend mainly on the total amount of CO2 and other greenhouse gases emitted as a result of human activities.

Since the mid-1800s, scientists have known that CO2 is one of the main greenhouse gases of importance to Earth’s energy balance. Direct measurements of CO2 in the atmosphere and in air trapped in ice show that atmospheric CO2 increased by about 40% from 1800 to 2012. Measurements of different forms of carbon (isotopes, see Question 3) reveal that this increase is due to human activities. Other greenhouse gases (notably methane and nitrous oxide) are also increasing as a consequence of human activities. The observed global surface temperature rise since 1900 is consistent with detailed calculations of the impacts of the observed increase in atmospheric CO2 (and other human-induced changes) on Earth’s energy balance.

Different influences on climate have different signatures in climate records. These unique fingerprints are easier to see by probing beyond a single number (such as the average temperature of Earth’s surface), and looking instead at the geographical and seasonal patterns of climate change. The observed patterns of surface warming, temperature changes through the atmosphere, increases in ocean heat content, increases in atmospheric moisture, sea level rise, and increased melting of land and sea ice also match the patterns scientists expect to see due to rising levels of CO2 and other human-induced changes (see Question 5).

The expected changes in climate are based on our understanding of how greenhouse gases trap heat. Both this fundamental understanding of the physics of greenhouse gases and fingerprint studies show that natural causes alone are inadequate to explain the recent observed changes in climate. Natural causes include variations in the Sun’s output and in Earth’s orbit around the Sun, volcanic eruptions, and internal fluctuations in the climate system (such as El Niño and La Niña). Calculations using climate models (see infobox, p.20) have been used to simulate what would have happened to global temperatures if only natural factors were influencing the climate system. These simulations yield little warming, or even a slight cooling, over the 20th century. Only when models include human influences on the composition of the atmosphere are the resulting temperature changes consistent with observed changes.

In nature, CO2 is exchanged continually between the atmosphere, plants and animals through photosynthesis, respiration, and decomposition, and between the atmosphere and ocean through gas exchange. A very small amount of CO2 (roughly 1% of the emission rate from fossil fuel combustion) is also emitted in volcanic eruptions. This is balanced by an equivalent amount that is removed by chemical weathering of rocks. The CO2 level in 2012 was about 40% higher than it was in the nineteenth century. Most of this CO2 increase has taken place since 1970, about the time when global energy consumption accelerated. Measured decreases in the fraction of other forms of carbon (the isotopes 14C and 13C) and a small decrease in atmospheric oxygen concentration (observations of which have been available since 1990) show that the rise in CO2 is largely from combustion of fossil fuels (which have low 13C fractions and no 14C).

Deforestation and other land use changes have also released carbon from the biosphere (living world) where it normally resides for decades to centuries. The additional CO2 from fossil fuel burning and deforestation has disturbed the balance of the carbon cycle, because the natural processes that could restore the balance are too slow compared to the rates at which human activities are adding CO2 to the atmosphere. As a result, a substantial fraction of the CO2 emitted from human activities accumulates in the atmosphere, where some of it will remain not just for decades or centuries, but for thousands of years. Comparison with the CO2 levels measured in air extracted from ice cores indicates that the current concentrations are higher than they have been in at least 800,000 years (see Question 6).

The observed warming in the lower atmosphere and cooling in the upper atmosphere provide us with key insights into the underlying causes of climate change and reveal that natural factors alone cannot explain the observed changes. In the early 1960s, results from mathematical/physical models of the climate system first showed that human-induced increases in CO2 would be expected to lead to gradual warming of the lower atmosphere (the troposphere) and cooling of higher levels of the atmosphere (the stratosphere). In contrast, increases in the Sun’s output would warm both the troposphere and the full vertical extent of the stratosphere.

At that time, there was insufficient observational data to test this prediction, but temperature measurements from weather balloons and satellites have since confirmed these early forecasts. It is now known that the observed pattern of tropospheric warming and stratospheric cooling over the past 30 to 40 years is broadly consistent with computer model simulations that include increases in CO2 and decreases in stratospheric ozone, each caused by human activities. The observed pattern is not consistent with purely natural changes in the Sun’s energy output, volcanic activity, or natural climate variations such as El Niño and La Niña. Despite this agreement between the global-scale patterns of modelled and observed atmospheric temperature change, there are still some differences. The most noticeable differences are in the tropical troposphere, where models currently show more warming than has been observed, and in the Arctic, where the observed warming of the troposphere is greater than in most models.

All major climate changes, including natural ones, are disruptive. Past climate changes led to extinction of many species, population migrations, and pronounced changes in the land surface and ocean circulation. The speed of the current climate change is faster than most of the past events, making it more difficult for human societies and the natural world to adapt. The largest global-scale climate variations in Earth’s recent geological past are the ice age cycles (see infobox, p.B4), which are cold glacial periods followed by shorter warm periods [Figure 3]. The last few of these natural cycles have recurred roughly every 100,000 years. They are mainly paced by slow changes in Earth’s orbit which alter the way the Sun’s energy is distributed with latitude and by season on Earth.

These changes alone are not sufficient to cause the observed magnitude of change in temperature, nor to act on the whole Earth. Instead they lead to changes in the extent of ice sheets and in the abundance of CO2 and other greenhouse gases which amplify the initial temperature change and complete the global transition from warm to cold or vice versa. Recent estimates of the increase in global average temperature since the end of the last ice age are 4 to 5 °C (7 to 9 °F). That change occurred over a period of about 7,000 years, starting 18,000 years ago. CO2 has risen by 40% in just the past 200 years, contributing to human alteration of the planet’s energy budget that has so far warmed Earth by about 0.8 °C (1.4 °F). If the rise in CO2 continues unchecked, warming of the same magnitude as the increase out of the ice age can be expected by the end of this century or soon after. This speed of warming is more than ten times that at the end of an ice age, the fastest known natural sustained change on a global scale.

The present level of atmospheric CO2 concentration is almost certainly unprecedented in the past million years, during which time modern humans evolved and societies developed. The atmospheric CO2 concentration was however higher in Earth’s more distant past (many millions of years ago), at which time palaeoclimatic and geological data indicate that temperatures and sea levels were also higher than they are today. Measurements of air in ice cores show that for the past 800,000 years up until the 20th century, the atmospheric CO2 concentration stayed within the range 170 to 300 parts per million (ppm), making the recent rapid rise to nearly 400 ppm over 200 years particularly remarkable [figure 3]. During the glacial cycles of the past 800,000 years both CO2 and methane have acted as important amplifiers of the climate changes triggered by variations in Earth’s orbit around the Sun.

As Earth warmed from the last ice age, temperature 7 continued 10 Climate Change n Q&A Is there a point at which adding more CO2 will not cause further warming? No. Adding more CO2 to the atmosphere will cause surface temperatures to continue to increase. As the atmospheric concentrations of CO2 increase, the addition of extra CO2 becomes progressively less effective at trapping Earth’s energy, but surface temperature will still rise. Our understanding of the physics by which CO2 affects Earth’s energy balance is confirmed by laboratory measurements, as well as by detailed satellite and surface observations of the emission and absorption of infrared energy by the atmosphere. Greenhouse gases absorb some of the infrared energy that Earth emits in so-called bands of stronger absorption that occur at certain wavelengths. Different gases absorb energy at different wavelengths. CO2 has its strongest heat-trapping band centred at a wavelength of 15 micrometres (millionths of a metre), with wings that spread out a few micrometres on either side.

There are also many weaker absorption bands. As CO2 concentrations increase, the absorption at the centre of the strong band is already so intense that it plays little role in causing additional warming. However, more energy is absorbed in the weaker bands and in the wings of the strong band, causing the surface and lower atmosphere to warm further. and CO2 started to rise at approximately the same time and continued to rise in tandem from about 18,000 to 11,000 years ago. Changes in ocean temperature, circulation, chemistry and biology caused CO2 to be released to the atmosphere, which combined with other feedbacks to push Earth into an even warmer state. For earlier geological times, CO2 concentrations and temperatures have been inferred from less direct methods. Those suggest that the concentration of CO2 last approached 400 ppm about 3 to 5 million years ago, a period when global average surface temperature is estimated to have been about 2 to 3.5°C higher than in the pre-industrial period. At 50 million years ago, CO2 may have reached 1000 ppm, and global average temperature was probably about 10°C warmer than today. Under those conditions, Earth had little ice, and sea level was at least 60 metres higher than current levels.

During El Niño events, global average temperatures tend to be warmer than normal, while during La Niña events, temperatures tend to be cooler than normal. Since 1950, both the cooler-than-normal La Niña periods and the warmer-than-normal El Niño periods have been warming over time. This shows that this natural cycle appears to be superimposed on a longer-term warming trend.

Earth’s lower atmosphere is becoming warmer and moister as a result of human-emitted greenhouse gases. This gives the potential for more energy for storms and certain severe weather events. Consistent with theoretical expectations, heavy rainfall and snowfall events (which increase the risk of flooding) and heatwaves are generally becoming more frequent. Trends in extreme rainfall vary from region to region: the most pronounced changes are evident in North America and parts of Europe, especially in winter. Attributing extreme weather events to climate change is challenging because these events are by definition rare and therefore hard to evaluate reliably, and are affected by patterns of natural climate variability.

For instance, the biggest cause of droughts and floods around the world is the shifting of climate patterns between El Niño and La Niña events. On land, El Niño events favour drought in many tropical and subtropical areas, while La Niña events promote wetter conditions in many places, as has happened in recent years. These short-term and regional variations are expected to become more extreme in a warming climate. There is considerable uncertainty about how hurricanes are changing because of the large natural variability and the incomplete observational record. The impact of climate change on hurricane frequency remains a subject of ongoing studies. While changes in hurricane frequency remain uncertain, basic physical understanding and model results suggest that the strongest hurricanes (when they occur) are likely to become more intense and possibly larger in a warmer, moister atmosphere over the oceans. This is supported by available observational evidence in the North Atlantic. Some conditions favourable for strong thunderstorms that spawn tornadoes are expected to increase with warming, but uncertainty exists in other factors that affect tornado formation, such as changes in the vertical and horizontal variations of winds.

Land and submarine volcanoes emit about 260 million metric tons of CO2 per year, researchers estimate. Human use of fossil fuels and CO2 emissions through land-use changes deliver more than

30 billion metric tons of the gas a year to the atmosphere – more than 100 times the annual emissions from volcanoes.

Without greenhouse gases the temperature on Earth would average 0 degrees F. With the greenhouse effect, the average temperature on Earth is 59 degrees F.

Electricity accounted for 32 percent of total US greenhouse gas emissions in 2012. The majority of that came from burning coal. Transportation is the second largest source of greenhouse gas emissions in the US. [Editor’s note: This response has been updated for clarification. Electricity accounted for 32 percent of total US greenhouse gas emissions in 2012. For just carbon dioxide emissions, the sector accounted for 38 percent of US emissions. In either case, it was the largest source of emissions in 2012.]

The average global sea level has risen 6.7 inches, or 17 centimeters, in the past century. However, the rate of change has doubled in the last decade. Between 1870 and 2000, the sea level rose at an average of 1.70 millimeters a year. From 1993-present it has risen at an average of 3.17 millimeters a year. This is caused by thermal expansion caused by warmer ocean water and the melting of glaciers and the polar ice caps. Sea-level changes vary widely by location. The East coast of the US is a hot spot for sea-level changes, which could impact major US cities.

In June 2014, scientists recorded the largest Antarctic sea ice extent ever. The sea ice covered about 15.26 million square kilometers. This surpassed the previous record, set in 2010, by 260,000 square kilometers. Some scientists see evidence that the air around Antarctica is warming, and warmer air can hold more moisture. That moisture leads to more snow falling on the ocean around Antarctica, which makes the ocean less salty and dense. Less salty water is able to freeze at a higher temperature.

1978 was the first time satellites were used to observe ice at the Arctic. Since then, the yearly minimum sea ice extent during the summer melt season has decreased by 40 percent. This has increased the amount of open water (lower albedo than ice) available to absorb sunlight and return it to the atmosphere later as heat. This change in albedo has has amplified the warming in the Arctic. [Editor’s note: The question has been updated to specify “annual minimum” of Arctic sea ice.]

1998 is the only year from the 20th century to be one of the 10 hottest years ever recorded. The other nine are years from the 21st century. Here are the top 10 hottest years on record, starting with the hottest: 2010, 2005, 1998, 2013, 2003, 2002, 2006, 2009, 2007, 2004, 2012.

In January 2015, NASA and NOAA announced that 2014 was the hottest on record, although scientists added that the margin of error is such that 2014, 2010, and 2005 are effectively statistically tied for first place

Ocean acidification: Oceans have absorbed about a third of the carbon dioxide created from human activities, decreasing the pH level. The ocean holds about 50 times more carbon than the atmosphere. Due to acidification, less calcium carbonate is available for building structures such as shells or coral reefs. Other effects include lower growth rates, reduce the immune responses among some species.

20 tons of carbon dioxide is the amt of ave American emittance annualy: When national emissions are calculated on a per-person basis, the average American consumes goods and services that generate about 19.74 tons of CO2 per year, according to the United Nations Statistics Division. Qatar tops the list of per capita emitters, with the average Qatari spewing more than 55 tons of CO2 into the atmosphere. On a national basis, China is the top CO2 emitter, followed by the US, India, Russia, and Japan, based on 2012 emissions estimates.

The ozone hole refers to destruction of ozone molecules in the stratosphere, mainly concentrated over Antarctica. A smaller, less dramatic hole appear over the Arctic. Ozone has thinned due mainly to fluorine-, chlorine-, and bromine-based industrial compounds. These were incorporated into widely used products like refrigerants, propellants for spray cans, and foam furniture cushions. The decline in ozone over Antarctic appears to have been arrested in the early to mid 1990s, and its size has been trending smaller since the mid 2000s.

The ozone hole refers to destruction of ozone molecules in the stratosphere, mainly concentrated over Antarctica. A smaller, less dramatic hole appear over the Arctic. Ozone has thinned due mainly to fluorine-, chlorine-, and bromine-based industrial compounds. These were incorporated into widely used products like refrigerants, propellants for spray cans, and foam furniture cushions. The decline in ozone over Antarctic appears to have been arrested in the early to mid 1990s, and its size has been trending smaller since the mid 2000s.

400 ppm: This is the highest concentration of CO2 the atmosphere has held in at least 800,000 years and more likely in 20 million years. Scientists expect the atmosphere to reach that average level on an annual basis next year. CO2 emissions are exceeding levels that would have provided a 50-50 chance of holding the increase in global average temperatures to about 2 degrees Celsius by 2100.

Over the past 30 to 40 years, as the troposphere (the major layer of the atmosphere closest to the surface), resumed warming after a 30- to 40-year pause, the stratosphere has cooled. The main reason is that fluorine-, chlorine-, and bromine-based industrial compounds have destroyed stratospheric ozone, which is a greenhouse gas. But the stratosphere also has been cooling because greenhouse gases in the troposphere have trapped more heat there.

Since 1900, the temperature of the atmosphere has risen 1.4 degrees F. Each of the last three decades has been warmer than any other decade.

From 1800 to 2012, the amount of atmospheric CO2 has increased

: Since pre-industrial times, the amount of carbon dioxide in the atmosphere has increased by 40 percent. Half of that increase has come since 1970. Additionally, the amount of methane in the atmosphere has increased by 150 percent.

Plants turn carbon dioxide into sugars and starches during photosynthesis, locking the carbon up in their tissues. On average, during their lifetimes plants return to the atmosphere about half of the CO2 they absorb. When they die and decompose, virtually all of their carbon returns to the atmosphere as CO2. If plants (or animals) are buried before they can decompose on the surface and remain buried, heat and pressure over millions of years turn them into deposits of coal, oil, and gas. CO2 from coal burned in a power plant today represents a return to the atmosphere of carbon long sequestered deep underground, away from the climate system.

The Earth’s surface absorbs the sun’s visible light and emits infrared radiation back toward space. Greenhouse gases absorb and re-emit the infrared radiation in all directions, including back toward Earth.

About 30 percent of the sun’s visible light is reflected by clouds, atmospheric particles, snow, and ice. That leaves 70 percent to be absorbed by the oceans, land, and plant cover to be returned to the atmosphere as heat. This relative reflectiveness, or albedo, also plays a role in keeping cities warmer than the surrounding countryside as dark roofs and large areas covered with asphalt – surfaces with low albedo – contribute to what is called the urban heat-island effect.

Methane is more efficient than carbon dioxide at trapping heat. But the atmosphere contains much less methane than CO2, which stays in the atmosphere much longer. It takes about a decade for a fresh methane molecule to leave the atmosphere. A fresh CO2 molecule can stick around for millenniums.

Tyndall’s paper On the Absorption and Radiation of Heat by Gases and Vapours, and on the Physical Connexion of Radiation, Absorption, and Conduction in 1861, was the first to establish, if shakily, that CO2, water vapor, and other gases had radiative properties, although others had speculated similarly before.

Acute myocardial infarction; imbalance during ischemia-reperfusion ; mitochondrial energy adaption in cancer, obesity and metabolic disorders

Acute myocardial infarction is characterized by changes in biochemical properties during ischemia and reperfusion. The heart can survive a short period of ischemia by reducing myocardial contractility, increasing glucose uptake, and switching metabolism to glycolysis.
However, considering that the heart is one of the most energy-demanding tissues in the body, sustained oxygen and nutrient deprivation results in irreversible damage. Thus, reperfusion of the ischemic heart is a prerequisite for survival.

Paradoxically, reperfusion can further increase the myocardial damage that occurs during ischemia. The severity of reperfusion injury depends on the duration of the preceding ischemia and the effectiveness of blood flow during reperfusion. Several lines of evidence demonstrate that reperfusion injury is directly associated with cardiac mitochondrial dysfunction and increased ROS and RNS generation.

An imbalance of oxidants and antioxidants resulting in increased levels of ROS, RNS, or both can result in damage to lipids, proteins, carbohydrates, and DNA.
ROS are oxygen radicals generated in the body due to exposure from polluted air

Hearse et al. noted that reperfusion of isolated hearts after ischemia resulted in abrupt cardiomyocyte death. Following this paper, several studies showed that ischemia reperfusion is associated with a burst of H2O2, O2•;−, NO•, and ONOO−, but the exact mechanism of their generation is debated.
Although some ROS may be generated by NADPH oxidase and xanthine oxidase, it is likely that complexes I and III of the mitochondrial respiratory chain are the main sources of ROS during myocardial ischemia reperfusion.

In fact, studies using mitochondrial respiratory inhibitors show that the electron leak along the oxidative phosphorylation most likely occurs at the Fe-S centers of complex I and at some components of complex III.
During the early stages of reperfusion, ROS generation levels increase drastically. Interestingly, low amounts of ROS generated by mitochondria during brief and intermittent episodes of ischemia, termed ischemic preconditioning, significantly protect the heart against prolonged ischemia.

Dietary antioxidants are substances that have been shown to decrease the effects of ROS and RNS in humans.
Redox (reduction-oxidation) reactions include all chemical reactions in which atoms have their oxidation state changed. This can be either a simple redox process, such as the oxidation of carbon to yield carbon dioxide (CO2) or the reduction of carbon by hydrogen to yield methane (CH4), or a complex process such as the oxidation of glucose (C6H12O6) in the human body through a series of complex electron transfer processes.

Redox reactions are concerned with the transfer of electrons between species. The term comes from the two concepts of reduction and oxidation. It can be explained in simple terms:
• Oxidation is the loss of electrons or an increase in oxidation state by a molecule, atom, or ion.
• Reduction is the gain of electrons or a decrease in oxidation state by a molecule, atom, or ion.

Although oxidation reactions are commonly associated with the formation of oxides from oxygen molecules, these are only specific examples of a more general concept of reactions involving electron transfer.

Redox reactions, or oxidation-reduction reactions, have a number of similarities to acid–base reactions. Like acid–base reactions, redox reactions are a matched set, that is, there cannot be an oxidation reaction without a reduction reaction happening simultaneously. The oxidation alone and the reduction alone are each called a half-reaction, because two half-reactions always occur together to form a whole reaction. When writing half-reactions, the gained or lost electrons are typically included explicitly in order that the half-reaction be balanced with respect to electric charge.

TABLE 1 Examples of Reactive Oxygen and Nitrogen Species
Name Formula Comments
Superoxide O2- An oxygen-centered radical. Has limited reactivity.
Hydroxyl OH• A highly reactive oxygen-centered radical. Very reactive indeed: Attacks all molecules in the human body.
Peroxyl, alkoxyl RO2•, RO• Oxygen-centered radicals formed (among other routes) during the breakdown of organic peroxides.
Oxides of nitrogen NO•, NO2• Nitric oxide (NO•) is formed in vivo from the amino acid L-arginine. Nitrogen dioxide (NO2•) is made when NO reacts with O2 and is found in polluted air and smoke from burning organic materials (e.g., cigarette smoke).

SOURCE: Adapted from Halliwell, 1996, with permission; © International Life Sciences Institute, Washington, D.C.

Mitochondrial function is fundamental to metabolic homeostasis. In addition to converting the nutrient flux into the energy molecule ATP, the mitochondria generate intermediates for biosynthesis and reactive oxygen species (ROS) that serve as a secondary messenger to mediate signal transduction and metabolism.
Alterations of mitochondrial function, dynamics, and biogenesis have been observed in various metabolic disorders, including aging, cancer, diabetes, and obesity. However, the mechanisms responsible for mitochondrial changes and the pathways leading to metabolic disorders remain to be defined.
In the last few years, tremendous efforts have been devoted to addressing these complex questions and led to a significant progress. In a timely manner, the Forum on Mitochondria and Metabolic Homeostasis intends to document the latest findings in both the original research article and review articles, with the focus on addressing three major complex issues:
(1) mitochondria and mitochondrial oxidants in aging—the oxidant theory (including mitochondrial ROS) being revisited by a hyperfunction hypothesis and a novel role of SMRT in mitochondrion-mediated aging process being discussed;
(2) impaired mitochondrial capacity (e.g., fatty acid oxidation and oxidative phosphorylation [OXPHOS] for ATP synthesis) and plasticity (e.g., the response to endocrine and metabolic challenges, and to calorie restriction) in diabetes and obesity;
(3) mitochondrial energy adaption in cancer progression—a new view being provided for H+-ATP synthase in regulating cell cycle and proliferation by mediating mitochondrial OXPHOS, oxidant production, and cell death signaling.
It is anticipated that this timely Forum will advance our understanding of mitochondrial dysfunction in metabolic disorders.
Antioxidants. Redox Signal. 00, 000–000.

Measurement of Quantities in Foods
In order to meet the definition of a dietary antioxidant proposed here, the dietary intakes of the nutrient or food component must be able to be calculated from available national databases. These databases include the U.S. Department of Agriculture’s National Nutrient Databank, the Canadian Nutrient File, and other databases that contain a nationally representative sample of foods commonly eaten in the United States or Canada and that report concentrations for the antioxidant of interest and others. It is recognized that limitations exist in the use of food composition databases to accurately estimate intakes.
Decreased Adverse Effects of Some ROS and RNS
In order to meet the definition of a dietary antioxidant proposed here, the nutrient or food component must decrease the adverse effects of some ROS and RNS (see Table 1 for examples of ROS and RNS). An explanation of the biochemical and physiological mechanisms of these adverse effects follows.
Role of ROS and RNS in Health and Disease
ROS and RNS are produced metabolically by the body. It has been estimated that about 1 to 3 percent of the oxygen we utilize goes to make ROS. In addition, exposure to UV radiation or to air pollutants such as cigarette smoke (which contains oxidants) or ozone can cause the body to increase the levels of reactive radical species.

ROS is a collective term that includes several oxygen radicals—superoxide (O2•-) and its protonated form, hydroperoxyl (HO2•), hydroxyl (OH•), peroxyl (RO2•), alkoxyl (RO•)—and nonradicals—hydrogen peroxide (H2O2), hypochlorous acid (HOCl), ozone (O3), and singlet oxygen (O2)—that are oxidizing agents or are easily converted into radicals. RNS includes nitric oxide (NO•), peroxynitrite (ONOO-), and peroxynitrous acid (ONOOH).
Various compounds in the human body generate free radicals in their metabolism. Examples are catecholamines and compounds found in the mitochondrial electron-transport chain.
In addition, activated phagocytes produce ROS as one of the defense mechanisms they use to kill microbes. Thus, in this situation, ROS are used by the body as a defense mechanism against infection.
An imbalance of oxidants and antioxidants resulting in increased levels of ROS, RNS, or both can result in damage to lipids, proteins, carbohydrates, and DNA.
A considerable body of biological evidence shows that ROS and RNS can damage cells and other body components and could in theory contribute to dysfunction and disease states.
It has been postulated that oxidative damage caused by increased levels of production of ROS or RNS may contribute to the development of many chronic diseases, including age-related eye disease, atherosclerosis, cancer, coronary heart disease, diabetes, inflammatory bowel disease, neurodegenerative diseases, respiratory disease, and rheumatoid arthritis.

Antioxidant Mechanisms
The mechanisms of antioxidant action for decreasing the adverse effects of ROS or RNS are varied. They include (1) decreasing ROS or RNS formation; (2) binding metal ions needed for catalysis of ROS generation; (3) scavenging ROS, RNS, or their precursors; (4) up-regulating endogenous antioxidant enzyme defenses; (5) repairing oxidative damage to biomolecules, such as glutathione peroxidases or specific DNA glycosylases; and (6) influencing and up-regulating repair enzymes.
Some antioxidants remove free radicals by reacting directly with them in a noncatalytic manner before the radicals react with other cell components. For example, vitamin E inhibits lipid peroxidation by scavenging radical intermediates in the radical chain reaction with polyunsaturated fatty acids.
The effectiveness of each dietary antioxidant depends on which ROS or RNS is being scavenged, how and where they are generated, the accessibility of the antioxidants to this site, and what target of damage, or oxidizable substrate, is involved.
Antioxidant defense mechanisms include not only low-molecular-weight compounds, but also some antioxidant defense systems in the human body that are enzymatic, such as: (1) superoxide dismutase enzymes, which remove superoxide (O2•-) by accelerating its conversion to H2O2 and O2; (2) glutathione peroxidases, which convert H2O2 to water and O2 and which convert various hydroperoxides to harmless compounds; and (3) catalase, which converts H2O2 to water and O2 but only functions at relatively high concentrations of the ROS.

Connie Dello Buono ;


Where do we stand on our fight against cancer causing substances?

We keep adding a list of these carcinogens or toxins each year. We have produced and manufactured foods in the factory in greater quantities and have to rely on so many chemicals.  Educating the public about the hazards of these carcinogens is very slow and tricky.  We have seen an increase in number of women with hysterectomies and breast/ovarian cancers. And we also have seen an increase in autism and Alzheimer’s disease.

We have to educate the public to:

  1. Wash vegtables and fruits (pesticide laden) with salt water or diluted vinegar.
  2. Stay away from toxic substances at home, preserved and packaged foods, materials in our foods, chemicals in our environment and other hidden toxins.
  3. Eat more fiber in the hopes that fiber can encapsulate the fat, sugar and toxins out of our bodies.
  4. Use organic, whole foods and less preserved food and more in its natural form.
  5. Live in a city that is not polluted and with well controlled hazardous substances to man and the environment.
  6. Stay at normal weight, reduce excess fat and excessive use of medications or drugs, even cosmetics and hair dyes.
  7. Walk our talk at home and in the community we live. Educate others.

Most toxic substances are substances that are persistent, bioaccumulative and toxic. These are substances that do not easily break down, instead they build up in nature and in the fatty tissue of mammals, with a potential to cause serious and long-term irreversible effects. The more fat we have in our body, the more our body is susceptible to storing carcinogens.  We hope that the recent research on the number of gene expressions related to cancer can shed light to how our body or personalized medicine can combat cancer.

Today, many women have hysterectomies and other form of reproductive cancer.  From the P65 list (created from 1987 to present, updated yearly), a total of 867 substances are listed as carcinogenic for reproductive and developmental health of growing embryo with 546 of these chemicals as specific contributor to cancer.  In 2011, there are 26 added carcinogens from the P65 list.


The following are a short list of carcinogens or toxins to man and the environment.

Obesity and Autism

Women who are obese and/or have diabetes or high blood pressure during pregnancy may be about 60% more likely to have babies with autism, a new study suggests. While the new research points to an association between mom’s health during pregnancy and autism, it’s important to note that “we can’t really draw causal links,” says researcher Paula Krakowiak. She is a PhD candidate in epidemiology at the University of California, Davis.


A 1988 survey published by the Foundation for Advancements in Science and Education also found styrene in human fatty tissue with a frequency of 100% at levels from 8 to 350 nanograms/gram (ng/g). The 350 ng/g level is one third of levels known to cause neurotoxic symptoms.[5] determined that Styrofoam drinking leach Styrofoam into the liquids they contain. The cups apparently lose weight during the time they are at use. The studies showed that tea with lemon produced the most marked change in the weight of the foam cup


“Are Styrene Food and Beverage Containers A Health Hazard?,” Institute for Local Self-Reliance, Washington, DC, August 15, 1990.
Brian Lipsett, “Areas of Expertise Pertaining to McDonald’s Corp..”
K. Figge, “Migration of Additives from Plastic Films into Edible Oils and Fat Stimulants,” Food Cosmet Toxicol, December 10, 1972, Vol. 6, pages 815 828.
B.J. Dowty, J.L. Laseter, and J. Storet, “Ther Transplacental Migration and Accumulation in Blood of Volatile Organic Constituents,” Pediatric Research, Vol. 10, pages 696-701, 1976.
“Polystyrene Fact Sheet,” Foundation for Advancements in Science and Education, Los Angeles, California.

According to a Foundation for Achievements in Science and Education fact sheet, long term exposure to small quantities of styrene can cause neurotoxic (fatigue, nervousness, difficulty sleeping), hematological (low platelet and hemoglobin values), cytogenetic (chromosomal and lymphatic abnormalities), and carcinogenic effects.[1,2] In 1987, the International Agency for Research on Cancer, Lyon, France, reclassified styrene from a Groups 3 (not classifiable as to its carcinogenicity) to a Group 2B substance (possibly carcinogenic to humans).

Although there is evidence that styrene causes cancer in animals, it has not yet been proven to cause cancer in humans. Styrene primarily exhibits its toxicity to humans as a neurotoxin by attacking the central and peripheral nervous systems. The accumulation of these highly lipid-soluble (fat-soluble) materials in the lipid-rich tissues of the brain, spinal cord, and peripheral nerves is correlated with acute or chronic functional impairment of the nervous system.

For example, women exposed to low concentrations of styrene vapors in the workplace are known to have a variety of neurotoxic and menstrual problems. A Russian study of 110 women exposed to styrene vapors at levels about 5 mg/m3 demonstrated menstrual disorders, particularly perturbations of the menstrual cycle and a hypermenorrhea (unusually heavy flow of menses during the menstrual cycle) syndrome. Styrene- exposed women often suffered from metabolic disturbances occurring during pregnancy.

The root cause of the build up of the toxin, styerene, is not the answer to our problem but the protection of our bodies against the onslaught of these toxins is far more important. Can a strong immune system help? What about lifestyle changes?


Dioxins are a group of chemicals that form as unwanted byproducts from incomplete burning of household and industrial waste. They also can be produced during bleaching of paper pulp and the manufacture of certain chlorinated chemicals like polychlorinated biphenyls (PCBs), chlorinated phenols, chlorinated benzene and certain pesticides. Exhaust from vehicles, forest fires, and burning wood also releases dioxins into the air. Very small amounts of dioxins, that are not considered harmful, are present in bleached paper products including facial or toilet tissue, paper towels, and disposable diapers.

Dioxin exposure can cause a severe skin condition called chloracne, which results in small, pale yellow skin lesions that may last from weeks to years. Dioxins can cause short-term liver effects without any visible symptoms. Studies of people exposed to high levels of dioxins through occupation, accidents or military service do not suggest that adverse health affects will occur at low levels in the environment. A large historical study suggested workers exposed to dioxins for many years had increased cancer rates. However, other environmental factors may be related to the cancer. Studies have shown that reproductive, immune and nervous systems of the developing fetus and children are more susceptible to dioxins.

In animal studies, dioxins have caused nerve damage, birth defects, increased rates of miscarriages and changes to the immune system. Although the U.S. Environmental Protection Agency has classified dioxins as a probablehuman carcinogen (cancer causing chemical), there is not sufficient evidence to prove that dioxins cause cancer from exposure to the low levels normally found in the environment. One dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is listed as a known human carcinogen and all the others as probable human carcinogens.

Source:  Illinois Department of Public Health
Division of Environmental Health
525 W. Jefferson St.
Springfield, IL 62761
TTY (hearing impaired use only) 800-547-0466


In 1999, the draft Fox River clean-up proposal included a local cancer risk assessment for recreational anglers and subsistence anglers due primarily to consumption of fish containing PCBs. Using fish concentration data from 1990 on (and Walleye data from 1989 in Green Bay), the cancer risks were as high as 1.1 in a 100 for recreational anglers, and 1 in 67 for subsistence anglers. These risks are more than 1,000 times greater than the standard 1-in-a-million cancer risk level used by Wisconsin to regulate hazardous waste sites. These risks are 23 times higher than the cancer risks from fish-eating from Lake Winnebago, which the DNR considers a background level for PCBs (though it’s clear that Lake Winnebago fish are also contaminated.)

Reference: ThermoRetec. Feb. 1999. “Draft Feasibility Study, Lower Fox River, Wisconsin, Summary of Baseline Human Health and Ecological Risk Assessment.” Section 3.2.1.

Hazardous House Cleaners

In 1990, more than 4,000 toddlers under age four were admitted to hospital emergency rooms as a result of household cleaner-related injuries. That same year, 18,000 pesticide-related hospital emergency room admissions were reported with almost three-fourths for children age fourteen and under.

Methylene chloride, the propellant used in many aerosol products, is carcinogenic. Some products containing methylene chloride have been pulled from the market, but the carcinogen continues to be found in many consumer products such as spray paint and stripper.

 Cosmetic Toxins

Not a single cosmetic company warns consumers of the presence of carcinogens in its products – despite the fact that a number of common cosmetic ingredients are carcinogenic or carcinogenic precursors.

Some experts estimate that 20 percent of non-Hodgkin’s lymphoma cases among women are attributable to their use of hair dyes.

Source: Cancer Prevention Coalition c/o School of Public Health, M/C 922
University of Illinois at Chicago 2121 West Taylor Street  Chicago, IL 60612
(312) 996-2297, Fax: (312) 413-9898 Email:

Tobacco and tobacco smoke

Tobacco smoke is a major source of human exposure to polycyclic aromatichydrocarbons (PAHs). The concentration of PAHs in lung tissue would reflect an individual’s dose, and its variation could perhaps reflect cancer risk. Eleven PAHs were measured in 70 lung tissue samples from cancer-free autopsy donors by gas chromatography-mass spectrometry. There were 37 smokers and 33 nonsmokers as estimated by serum cotinine concentration. The sum of PAH concentrations was higher in smokers (P = 0.01), and there was a dose-response relationship for greater smoking (P < 0.01).

Smoking increased the concentration of five PAHs including benzo(a)pyrene, which increased ∼2-fold. The risk for increasing carcinogenic PAHs (odds ratio, 8.20; 95% confidence interval, 2.39–28.09) was 3-fold compared with noncarcinogenic PAHs (odds ratio, 2.61; 95% confidence interval, 0.75–9.12). A higher concentration of PAHs was detected in the lung tissue of males, although the estimated smoking was similar in males and females. Race was not associated with PAH concentrations overall, but PAH concentrations appeared to be higher in African-American males than in any other group. Age was weakly correlated with an increase in fluoranthene and pyrene. The measurement of PAHs in human lung tissue can be used to estimate the actual dose to the target organ.

Source:  Cancer Res September 1, 2001 61; 6367

More of us are relying on food containing endocrine disruptive chemicals such as synthetic hormones in meat, eggs and milk.

Sugar (High fructose corn syrup) and our Liver

The fructose component of sugar and H.F.C.S. is metabolized primarily by the liver, while the glucose from sugar and starches is metabolized by every cell in the body. Consuming sugar (fructose and glucose) means more work for the liver than if you consumed the same number of calories of starch (glucose). And if you take that sugar in liquid form — soda or fruit juices — the fructose and glucose will hit the liver more quickly than if you consume them, say, in an apple (or several apples, to get what researchers would call the equivalent dose of sugar). The speed with which the liver has to do its work will also affect how it metabolizes the fructose and glucose.

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance, which is now considered the fundamental problem in obesity, and the underlying defect in heart disease and in the type of diabetes, type 2, that is common to obese and overweight individuals. It might also be the underlying defect in many cancers.


However, further analysis within the Nurses’ Health Study indicates that there may be an association between consumption of sugar-sweetened beverages, other than fruit juices, and an increased risk of type 2 diabetes in women, possibly by providing excessive calories and large amounts of rapidly absorbable sugars (Schulze, 2004).

Reactive carbonyls also are elevated in the blood of individuals with diabetes and linked to the complications of that disease. Based on the study data, Ho estimates that a single can of soda contains about five times the concentration of reactive carbonyls than the concentration found in the blood of an adult person with diabetes.

Ho and his associates also found that adding tea components to drinks containing HFCS may help lower the levels of reactive carbonyls. The scientists found that adding epigallocatechin gallate (EGCG), a compound in tea, significantly reduced the levels of reactive carbonyl species in a dose-dependent manner when added to the carbonated soft drinks studied. In some cases, the levels of reactive carbonyls were reduced by half, the researchers say.

Source: This research was reported August 23 at the 234th national meeting of the American Chemical Society, during the symposium, “Food Bioactives and Nutraceuticals: Production, Chemistry, Analysis and Health Effects: Health Effects.” ScienceDaily (Aug. 23, 2007)

Endocrine-Disrupting Chemicals

There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health.

The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models.

Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use.

We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.

Source: Andrea C. Gore, Ph.D., The University of Texas at Austin, College of Pharmacy, 1 University Station, A1915, Austin, Texas 78712. E-mail:

BHA, stabilizes the petroleum wax in food products, is also a carcinogen.



From the 53 list, let’s take a look at asbestos.  Asbestos has been classified as a known human carcinogen (a substance that causes cancer) by the U.S. Department of Health and Human Services, the EPA, and the International Agency for Research on Cancer (2, 3, 7, 8). Studies have shown that exposure to asbestos may increase the risk of lung cancer and mesothelioma (a relatively rare cancer of the thin membranes that line the chest and abdomen). Although rare, mesothelioma is the most common form of cancer associated with asbestos exposure. In addition to lung cancer and mesothelioma, some studies have suggested an association between asbestos exposure and gastrointestinal and colorectal cancers, as well as an elevated risk for cancers of the throat, kidney, esophagus, and gallbladder (3, 4).

The following are 53 carcinogens from the National Toxicology Program, Department of Health and Human Services Report on Carcinogens, Twelfth Edition (2011)
Alcoholic Beverage Consumption………..
Analgesic Mixtures Containing Phenacetin (see Phenacetin and Analgesic Mixtures Containing Phenacetin)………..
Aristolochic Acids
Arsenic and Inorganic Arsenic Compounds…..
Benzidine (see Benzidine and Dyes Metabolized to Benzidine)….
Beryllium and Beryllium Compounds…
Bis(chloromethyl) Ether and Technical-Grade Chloromethyl Methyl Ether……
Cadmium and Cadmium Compounds..
1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (see Nitrosourea Chemotherapeutic Agents)…….
Chromium Hexavalent Compounds….
Coal Tars and Coal-Tar Pitches…………….
Coke-Oven Emissions…………..
Cyclosporin A………
Dyes Metabolized to Benzidine (Benzidine Dye Class) (see Benzidine and Dyes Metabolized to Benzidine)……………..
Estrogens, Steroidal
Hepatitis B Virus….
Hepatitis C Virus….
Human Papillomaviruses: Some Genital-Mucosal Types……………..
Methoxsalen with Ultraviolet A Therapy………
Mineral Oils: Untreated and Mildly Treated….
Mustard Gas………..
Neutrons (see Ionizing Radiation)………
Nickel Compounds (see Nickel Compounds and Metallic Nickel)..
Radon (see Ionizing Radiation)…………..
Silica, Crystalline (Respirable Size)……..
Solar Radiation (see Ultraviolet Radiation Related Exposures)……
Strong Inorganic Acid Mists Containing Sulfuric Acid..
Sunlamps or Sunbeds, Exposure to (see Ultraviolet Radiation Related Exposures)…..
Thorium Dioxide (see Ionizing Radiation)…….
Tobacco Smoke, Environmental (see Tobacco-Related Exposures)
Tobacco Smoking (see Tobacco-Related Exposures)…..
Tobacco, Smokeless (see Tobacco-Related Exposures)
Ultraviolet Radiation, Broad-Spectrum (see Ultraviolet Radiation Related Exposures).
Vinyl Chloride (see Vinyl Halides [selected])…
Wood Dust…………..
X-Radiation and Gamma Radiation (see Ionizing Radiation)………