Air Pollution

CANCER: Health effect of air and water pollution

Lela Gary, Margaret Mroziewicz, Altaf Ghori
August 2010

"From the right to know and the duty to inquire flows the obligation to act."
Sandra Steingraber

You are welcome and encouraged to share, copy and excerpt this report, provided it is referenced.

Introduction

Cancer does not discriminate.

It may affect any organ of our body and may develop into rare types of cancer as reported by Dr. John O'Connor in 2006 of the increased incidence of the bile duct cancer affecting the Native population living in the vicinity of the Alberta oil tar sands in Fort Chipewyan. Toxins from the tailing ponds travel downstream into the lake which provides the village with drinking water.
The new report released by Environment Canada, (http://www.ec.gc.ca/inrpnpri/default.asp?lang=en&n=CE124285-1) shows the mining operations at the oil sands released exorbitant amounts of pollutants into the air, including 70,658 tonnes of VOCs (Volatile Organic Compounds) which damage the function of human organs, and (carcinogens) polycyclic aromatic hydrocarbons which cause lung, skin and bladder cancer.

This report concentrates on Lung, Breast, and Brain Cancer.

Cancers are on the rise, many of which are linked to environmental and occupational exposures. The Canadian Cancer Society in their 2010 report estimate 173,800 new cases this year, up 2,800 from last year, and 76,200 deaths, up 900. Leukemias and lymphomas have been linked to petroleum products, including VOCs, dioxin-like chemicals, and other hydrocarbons. Biliary cancers have been linked to petroleum and to PAHs (Polycyclic Aromatic Hydrocarbons) chemicals in tar and soot. There are over 80,000 industrial chemicals in the environment but few are tested for their danger level and less emphasis has been given to their synergistic effect created, which is greater than its parts. Over 80% of “Priority substances” in emissions are toxins not reported. We are exposed to about 10,000 different chemicals a day.

Air pollution kills.
According to the Canadian Medical Association 90,000 Canadians will have died from the acute short-term effects of air pollution by 2031, with accumulative death toll of 800,000. Emissions in Canada grew by 26.6% from 1990 to 2005. Emissions from the transportation sector grew by 32.8% (48.8 million tonnes).
According to the International Energy Agency (IEA) Canada’s emissions would be 24% higher in 2020 than in 1990, as no policies have been introduced to ensure reduction of emissions. By contrast, US emissions would be 4% lower than 1990 and the European Union’s 20% lower based on their emissions targets.

The following are the most common carcinogens:

AsbestosFormaldehydeTrichlorethylene
BenzeneCadmiumMethylene Chloride
TetrachlorethyleneChromiumDiesel Fuel
Dioxins & Furans1,3 ButadienePesticides
PAHsMercury & LeadBenzopyrene

 

Lung Cancer

Canadians have a 1 in 11 chance of developing lung cancer, and a 1 in 13 chance of dying from it.1 Lung cancer accounts for 8% of all Canadian deaths being the second most common and the leading cause of cancer death (27% of all cancer mortalities).2 Although smoking is the primary cause of lung cancer, 25% of all cases worldwide are not attributed to smoking.3 Air pollution from industrial sources, power plants, and vehicle emissions is a prominent factor in causing lung cancer.

Scientific studies worldwide suggest that air pollution causes lung cancer. Fine particles (particularly PM2.5 and PM10), which are made up of hazardous materials (e.g. metals), and carcinogens PAHs (Polycyclic Aromatic hydrocarbons) also stick to their surface.4 And when inhaled, they may initiate lung cancer. Long-term studies have demonstrated the association between lung cancer and air pollution. A study in the US (with 500,000 participants in over 100 cities) assessed long-term exposure to fine particulates and lung cancer5, and that increased air pollution led to an increased risk for lung cancer mortality (for each 10-µg/m3 increase in fine particulate air pollution, lung cancer mortality increased by 8%). This effect was largest in non-smokers. The researchers concluded that there are no safe levels of air pollution, and as fine particulate air pollution increases, the risk of lung cancer mortality also increases. Lung cancer death rates can be reduced if air pollution is reduced.

Ten European countries (Sweden, Denmark, Norway, Netherlands, UK, France, Germany, Spain, Italy, Greece) were also part of a study (with over 500,000 study participants) to assess the role of air pollution in lung cancer in never smokers and ex-smokers.6 The study revealed that 5-7% of lung cancers in European non-smokers were due to high levels of air pollution from vehicles, specifically by nitrogen dioxide (NO2, an index of traffic pollution) or proximity to heavy traffic roads; but, due to strict NO2 thresholds used in their study, in reality, the percentage of lung cancers due to heavy pollution was likely higher than 5-7%. Smaller studies on urban air pollution and lung cancer, in Stockholm, Sweden, particularly from traffic(NO2) increased lung cancer risk.7 Likewise, a study in Denmark concurred on the association between traffic air pollution and lung cancer.8 In the Netherlands, scientists also reported an association of exposure to black smoke and traffic intensity with lung cancer incidence, particularly in people who had never smoked.9

Primary lung cancers (i.e. started in the lung) are divided into:
  • Small cell lung cancer
  • Non-small cell lung cancer, which includes:
    • Squamous cell carcinoma
    • Adenocarcinoma
    • Large cell carcinoma
Different types of lung cancers were reported in a study in Trieste, Italy, with respect to living in the polluted city center relative to a suburban area increased the risk of small cell and large cell lung cancer, while living in an industrial area increased the risk for adenocarcinoma9 and that lung cancer risk increased with increasing levels of air pollution. Exposure to metal air pollutants was associated with various types of lung cancer incidence in Texas, US10 Specifically, zinc was associated with primary and non-small cell lung cancers, and chromium and copper were associated with non-small cell lung cancer.

The effects of air pollution in lung cancer have also been studied in Asian cities. A study in Shizuoka, Japan, concluded that long-term exposure to traffic pollution (indicated by NO2) increased the risk of lung cancer mortality in non-smokers.12 Researchers in Taiwan showed a correlation between traffic-related air pollution (measured by nitrous oxides and carbon monoxide) and incidence of lung adenocarcinoma.13 An increased risk of lung cancer in women compared to men was reported in a study in seven Korean cities on long-term exposure to PM10, was significantly associated with only female lung cancer incidence and mortality.14 In Taiwan researchers used petrol station density as an indicator of exposure to gaseous petrol chemicals or vehicle emissions. The results of this study indicated a significant relationship between petrol station density and risk of lung cancer in females.15 Lung cancer is also linked to power plant emissions. Researchers in the United States used an air pollution index correlated with coal power-plant emissions, and found that the index correlated with lung cancer (among many other cancers).16 They warned that combustion of coal, diesel fuel and wood releases particles carrying PAHs, cause many types of cancers. Scientists in Spain also reported that proximity to fossil fuel power-plants was associated with increased lung cancer mortality.17

All of the above studies have ascertained the effect of air pollution from industrial sources, power plants and vehicles, on lung cancer and that lung cancer risk increases as air pollution increases. This prevalent and lethal disease can be reduced if air quality is improved.

 

Breast Cancer

1 in 9 women are expected to develop breast cancer in their lifetime
1 in 29 women are expected to die from it
1 in every 111 females alive on January 1, 2005 had been diagnosed with breast cancer in the previous 10 years5

About 22,000 women are diagnosed with breast cancer every year, as reported by the Canadian Breast Cancer Network, and bear huge financial burdens on top of the physiological challenges.

In both sexes the manifestation of breast cancer is similar suggesting a common origin of the disease.7 Mutations may be inherited or induced by chemical carcinogens.21 Route, timing, frequency of exposure to carcinogens contribute to the overall susceptibility to breast cancer development.1

A Scandinavian study of twins done in 2000 found that al¬though inherited factors accounted for 27% of breast can¬cer risk, 73% of the risk was linked to environmental factors, suggesting that environment plays a major role in determining risk.14 A 1991 study conducted on rural Asian women immigrating to the United States found that the daughters and granddaughters of these women had a higher chance of developing breast cancer. Within two generations, breast can¬cer rates of their offspring were as high as those of Western white women.20 Research has been done worldwide to prove that pollutants increase the risk of breast cancer in both women and men.1

Epidemiologic studies suggest 50% to 500% increases in risk in women exposed to pollutants such as polychlorinated biphenyls (PCBs), dichlorodipheny-ltrichloroethane (DDT), polycyclic aromatic hydrocarbons (PAHs), and chemical solvents.16 In 2007 Rudel et al published an article on environmental carcinogens causing the development of tumors in the mammary gland of animals. By compiling data from 450 primary epidemiology research articles from the International Agency for Research on Cancer (IARC), the U.S. National Toxicology Program (NTP), and other sources, 216 carcinogenic compounds were found. Chemicals were mutagenic and most caused tumors in multiple organs in animal species.16 Of the 216 chemicals on the list, 35 are outdoor pollutants (ambient) or indoor (residential) air, 25 have involved occupational exposures to more than 5000 women.16 Researchers found that risk assessment and regulatory documents have not been developed for these chemicals. 4

The evidence to date supports the association between breast cancer, PAHs and PCBs.3 PAHs are lipophilic chemical carcinogens mainly formed by incomplete combustion of fossil fuels that are absorbed into the fat cells of the body.10 Benzo[a]pyrene, a type of carcinogenic PAHs, has been shown to be activated by xenobiotic-metabolizing enzymes to highly mutagenic and carcinogenic metabolites that initiate cell transformation.10 If exposure to PAH is high or the detoxification pathway is insufficient, PAH-DNA adducts are formed, which increase the risk of breast cancer.18 Based on models of PAHs estimates attributed to vehicular traffic, it is reported that there is over a two-fold increase in risk for exposure for breast cancer.9

The Long Island Breast Cancer Study Project (LIBCSP) multi-institutional collaboration research in 2002 in Long Island, New York, observed a 50% elevation in the risk of breast cancer in relation to the highest amount of PAH-DNA adduct levels.10 A 2004 study in New York supported the data that PAHs increase the risk of developing breast cancer, indicated a 35% increase in breast cancer risk in individuals that lived in polluted locations.8 A 2003 study reported that higher levels of PAH-DNA adducts were found in individuals that lived in areas with high pollution compared to those that lived in less polluted locations.11 A 1996 study in New York recorded a higher risk of cancer associated with living in areas with air pollution from industrial facilities.13

Occupational exposure to gasoline and vehicular exhaust has been identified with elevated risk in both female and male breast cancer in individuals that work in these conditions. 12, 15 Organochlorine compounds, such as PCBs, chlorinated dioxins, furans, and pesticides, are frequently detected in food, soil, and dust.15 These chemicals concentrate up the food chain, and have been found in human breast milk and adipose tissue.3

Extensive evidence has been presented on the effect of air pollution on breast cancer by damaging DNA, promoting tumour growth, and increasing susceptibility by altering mammary gland development.15 Recognizing the effect of environmental chemicals on breast cancer will bring awareness to governments, the medical profession, and the public about the dangers these pollutants place on our health and economy. The government should act proactively to encourage safe environmental corporate practices and to improve public health policies.22

 

Brain Cancer

The link between air pollution and brain cancer has been reported in studies on both adults and children.

This report refers to the primary brain cancer regarding the effect of chemicals at the molecular level, excluding metastases. Brain tumours develop as a consequence of cellular genetic alterations that evade and destroy the immune system. Only a small proportion of brain tumours has been attributed to inherited predisposition, as is the case in other cancers, where only up to 6% is attributed to the genetic factor.

Brain tumours, most devastating of all cancers, can be developed through neurotrans- mitter misregulation. One of the symptoms is “Brain fog” also experienced by migraineurs exposed to high level of pollution. A common cause of brain fog is the reduction of oxygen to the brain from the effect of air toxics, especially the ultrafine particles (http://www.ecopolitics.ca/airpol/migraine.php.
Our inquiry for further research: Are migraineurs at a higher risk in developing brain tumours?

Breakdown of the nasal olfactory epithelial barrier contribute to brain inflammation by increasing the access of air pollution to the brain, both directly through the olfactory pathway and indirectly through the systemic circulation.1, 1a Chemical assaults on the brain, such as glutamate, NMDA, and formaldyhyde occur by neurotransmitters through the olfactory system, are implicated in brain-cell injury and death..2 ( Nasal olfactory and respiratory mucosae are targets for air pollutant-induced toxicity and carcinogenicity.) Formaldehyde, a colourless strong-smelling chemical that is used in building materials, household products, automobile tailpipe emissions, is a carcinogen that increases the risk of brain cancer and leukemia in individuals who have a prolonged exposure to this toxic.3

Another industrial pollutant, the carcinogen TCE (Trichloroethylene) has been detected in various human organs, brain, liver, etc.4 Additionally, neurological effects related to traffic air pollution in a study on the brain tissue of animals in Mexico City, indicated higher levels of nuclear factor-B activation and nitric oxide production and tumour necrosis factor (TNF: the presence of dead cells in the middle of the tumour) compared with the animals from non-polluted areas.

Drs. Keith Black and Julia Ljubimova in their research on brain tumours and air pollution at the Cedars Sinai Medical Center in California, observed that fine particle pollution passes through cell walls and triggers molecular changes to the same genes associated with brain cancer. Fine particles, like those in diesel soot, can switch on tumour genes that people inherit and jump-start the disease process and the destruction of the immune system.5 Studies have shown firefighters exposed to diesel exhaust in their fire stations are more likely to develop brain cancer than people in other occupations. Pollution particles enter through the damaged blood vessels and enter the brain walls, the blood brain barrier (BBB). The risk of cancer in firefighters examined in a study by the Division of Environmental and Occupational Medicine at the Mount Sinai School of Medicine in New York, noted the effect of carcinogens benzene, asbestos, PAHs, diesel exhaust, and formaldehyde have on prevalent cancers of brain and bladder, among others.14

The brain is particularly susceptible to toxins and free radical mediated insult, due to its inherent biochemical and physiological characteristics.6 In a study done in France on parental exposure to polycyclic aromatic hydrocarbons (PAH), which occurs primarily through air pollution, second hand smoke, and occupational exposure, increases the risk of all childhood brain tumours.7 Correspondingly, in a study by the Department of Environmental & Occupational Health at Emory University in Atlanta, Georgia, on the residential exposure to toxics during pregnancy, the researchers observed an extensive number of children diagnosed with brain cancer before 5 years of age and living within 1mile of a facility releasing mass carcinogens.8 In a 2009 study at the Division of Health Studies in Atlanta, Georgia, on parental exposure to pesticides and childhood brain cancer, they concluded that the exposures to herbicides from both residential and occupational sources had a significant elevated risk of brain cancer.9

To understand the cancer incidence due to airborne toxicants in anthropogenic pollution, an investigation in Indiana counties on the relationship between air emissions of volatile organic compounds (VOCs) and the incident of cancer, referred to strong correlations between VOC emissions and cancer of the brain, nervous system, and skin.10

Petroleum and petrochemical complexes have been identified for the significant excess deaths due to cancers, especially of the brain, bone, and bladder among children and adolescents in a residential district in Taiwan living within 3km of the facility.12 A follow-up case-control study was conducted in Taiwan from 1995 - 2005 regarding to residents' exposure to air emissions from petrochemicals. The subjects living in municipalities characterized by the highest levels of air pollution, had a statistically significant higher risk of developing brain cancer.13 Another study showed that genes associated with common brain tumours and degenerative brain diseases are more active in rat brains exposed to highway pollution for periods ranging from 2 weeks to 10 months.6,7

In contrast to the proven causes of hereditary syndromes or radiation, which account for a small proportion of cases, studies continue to associate brain cancer to workplace, personal, and residential exposures to carcinogenic toxics. Urban pollution has been identified in these studies to be a potential public health risk of great importance.15

 

CONCLUSION:

"Our lives begin to end the day we stay silent about the things that matter"
Martin Luther King Jr.

The long-term consequences of carcinogenic air and water chemicals of urban pollution should be incorporated in multidisciplinary research and promoted actively by the Department of Public Health. Little has been done to act on what we already know. The impact urban pollution has on our health should not be discussed endlessly with no determination of action. Nor should the government kowtow to industry and introduce amendments to “streamline” their environmental assessment processes. If the public can not combat the powers of industry or ineffective governments that contravene in the prevention of disease, the Chief Medical Officer must protect public health by developing strategies on health, environmental and social determinants.
Yet, in Ontario the limited powers of the Chief Medical Officer, under subsection (1) [86.3(2)] are counterproductive to the Health Protection and Promotion Act. (www.ecopolitics.ca/airpol/proposal_cmo.php)

Health Protection is defined as Prevention.
The current HPPA is inadequate to protect public health as it is based on Remedial Intervention. It fails its full implementation of the mandate in its rightful meaning, and it does not reflect the socio-economic costs to health and the legitimacy of human rights and social justice.

* * * * * *

NOTE!
Previous reports on health were presented to the Toronto Board of Health, in 1998 and 2003 respectively, when Drs. Ted Boadway, Director of Ontario Medical Association, and the late Sheela Basrur, Toronto Medical Officer of Health, were present.
The intent to present the above report to the Toronto Board of Health at the August 20, 2010 meeting, was refused by the Chair of the Toronto Board of Health , Councillor John Filion.

Bureaucracy marred by blind folly, benefits no one.

 

REFERENCES:

Lung Cancer

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2 Public Health Agency of Canada. Lung Cancer. Date modified: 2009-03-02. http://www.phac-aspc.gc.ca/cd-mc/cancer/lung_cancer-cancer_poumon-eng.php

3 Sun S, Schiller JH, Gazdar AF. Lung cancer in never smokers--a different disease. Nat Rev Cancer. 2007 Oct;7(10):778-90. http://www.ncbi.nlm.nih.gov/pubmed/17882278

4 Vineis P, Forastiere F, Hoek G et al. Outdoor air pollution and lung cancer: recent epidemiologic evidence. International Journal of Cancer. 2004;111:647-652. http://www3.interscience.wiley.com/cgi-bin/fulltext/108566716/PDFSTART

5 Pope CA 3rd, Burnett RT, Thun MJ et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 2002 Mar 6;287(9):1132-41. http://www.ncbi.nlm.nih.gov/pubmed/11879110

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7 Nyberg F, Gustavsson P, Järup L et al. Urban air pollution and lung cancer in Stockholm. Epidemiology. 2000 Sep;11(5):487-95. http://www.ncbi.nlm.nih.gov/pubmed/10955399

8 Raaschou-Nielsen O, Bak H, Sørensen M et al. Air pollution from traffic and risk for lung cancer in three Danish cohorts. Cancer Epidemiol Biomarkers Prev. 2010 May;19(5):1284-91. http://www.ncbi.nlm.nih.gov/pubmed/20447920

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11 Coyle YM, Minahjuddin AT, Hynan LS, Minna JD. An ecological study of the association of metal air pollutants with lung cancer incidence in Texas. J Thorac Oncol. 2006 Sep;1(7):654-61. http://www.ncbi.nlm.nih.gov/pubmed/17409932

12 Yorifuji T, Kashima S, Tsuda T, et al. Long-term exposure to traffic-related air pollution and mortality in Shizuoka, Japan. Occup Environ Med. 2010 Feb;67(2):111-7. http://www.ncbi.nlm.nih.gov/pubmed/19773277

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14 Hwang SS, Lee JH, Jung GW, Lim JH, Kwon HJ. Spatial analysis of air pollution and lung cancer incidence and mortality in 7 metropolitan cities in Korea. J Prev Med Public Health. 2007 May;40(3):233 http://www.ncbi.nlm.nih.gov/pubmed/17577079

15 Chang CC, Tsai SS, Chiu HF et al. Traffic air pollution and lung cancer in females in Taiwan: petrol station density as an indicator of disease development. J Toxicol Environ Health A. 2009;72(10):651-7. http://www.ncbi.nlm.nih.gov/pubmed/19308850

16 Grant WB. Air pollution in relation to U.S. cancer mortality rates: an ecological study; likely role of carbonaceous aerosols and polycyclic aromatic hydrocarbons. Anticancer Res. 2009 Sep;29(9):3537-45 http://www.ncbi.nlm.nih.gov/pubmed/19667146

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Saldiva, P.H.N. Lung Inflammation Induced by Concentrated Ambient Air Particles Is Related to Particle Composition. American Journal of Respiratory and Critical Care Medicine Vol 165. pp. 1610-1617, (2002) © 2002 American Thoracic Society. http://ajrccm.atsjournals.org/cgi/content/abstract/165/12/1610++

Breast Cancer

1 Bennett L. M., & Davis, B. J. (2002). Identification of mammary carcinogens in rodent bioassays. Environmental Molecular Mutagen 39(2-3), 150-157. http://www.ncbi.nlm.nih.gov/pubmed/11921183

2 Birnbaum, L. S. & Fenton, S. E. (2003). Cancer and Developmental Exposure to Endocrine Disruptors. Environmental Health Perspectives, 111(4), 389-393. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241417/

3 Brody, J. G., Moysich, K. B., Attfield, K. R., Beehler, G. P., Rudel, R. A. (2007). Environmental pollutants and breast cancer: epidemiologic studies. Cancer, 109(12), 2667-2711. http://www.ncbi.nlm.nih.gov/pubmed/17503436

4 Brody, J.G., & Rudel, R. A. (2008). Environmental pollutants and breast cancer: The evidence from animal and human studies. Breast Diseases: A Year Book Quarterly, 19(1), 17-19. http://library.silentspring.org/publications/pdfs/Brody_2008_BDQ.pdf

5 Canadian Cancer Society’s Steering Committee. Canadian Cancer Statistics 2009. Toronto: Canadian Cancer Society, 2009.

6 Cohn BA,Wolff MS, Cirillo PM, Sholtz RI. (2007) DDT and breast cancer in young women: new data on the significance of age at exposure. Environ Health Perspective 115, 1406-1414. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2022666/

7 Coyle, Y. M., Hynan, L. S., Euhus, D. M., & Minhajuddin, T. M. (2005). An Ecological Study of the Association of Environmental Chemicals in Breast Cancer Incidence in Texas. Breast Cancer Research and Treatment, 92, 107-114. http://www.ncbi.nlm.nih.gov/pubmed/15986119

8Gammon,M. D., Eng, S. M., Shantakumar, S., Gaudet, M. M., Teiteulbaum, S. L., Britton, J. A., Terry, M. B., Wang, L. W., Stellman, S. D., Beyea, J., Hatch, M., Kabat, G. C., Wolff, M. S., Levin, B., Neugut, A. I., & Santella, R. M. (2004). Polycyclic Aromatic Hyrocarbon-DNA adducts and Breast Cancer: A Pooled Analysis. Archives of Environmental Health, 59(12), 640-649. http://www.ncbi.nlm.nih.gov/pubmed/16789472

9 Gammon, M.D. & Santella, R.M. (2008). PAH, genetic susceptibility and breast cancer risk: An update from the Long Island Breast Cancer Study Project. European Journal of Cancer 44, 636-640. http://www.ncbi.nlm.nih.gov/pubmed/16789472

10 Gammon, M. D., Santella, R. M., Neugut, A. I. et al. (2002). Environmental toxins and breast cancer in Long Island. Polycyclic aromatic hydrocarbon DNA adducts. Cancer Epidemiology Biomarkers and Prevention, 11, 677-685. http://cebp.aacrjournals.org/content/11/8/677.full

11 Godschalk, R. W. L., Van Shooten, F., & Bartsch, H. (2003). A Critical Evaluation of DNA adducts as Biological Markers for Human Exposure to Polycyclic Aromatic Compounds. Journal of Biochemistry and Molecular Biology, 36(1), 1-11. http://jbmb.or.kr/jbmb/jbmb_files/%5B36-1%5D0301220008_001.pdf

12 Hansen J. Elevated risk for male breast cancer after occupational exposure to gasoline and vehicular combustion products. Am J Ind Med. 2000;37:349–352. http://www.ncbi.nlm.nih.gov/pubmed/10706746

13 Lewis-Michl EL, Melius JM, Kallenbach LR, et al. Breast cancer risk and residence near industry or traffic in Nassau and Suffolk Counties, Long Island, New York. Arch Environ Health. 1996;51:255–265. http://www.ncbi.nlm.nih.gov/pubmed/8757405

14 Lichtenstein, P., Holm, B. V., Verkasalo, P. K., Iliadou, A., Kaprio, J., Koskenvuo, M., et al. (2000). Environmental and heritable factors in the causation of cancer: Analyses of cohorts of twins from Sweden, Denmark, and Finland. New England Journal of Medicine, 343(2), 78-85. http://www.nejm.org/doi/full/10.1056/NEJM200007133430201

15 Petralia SA, Vena JE, Freudenheim JL, et al. Risk of premenopausal breast cancer in association with occupational exposure to polycyclic aromatic hydrocarbons and benzene. Scand J Work Environ Health. 1999;25:215–221. http://www.sjweh.fi/download.php?abstract_id=426&file_nro=1

16 Rudel R.A., Attfield K.R., Schifano J.N., & Brody J.G. (2007) Chemicals causing mammary gland tumors in animals signal new directions for epidemiology, chemicals testing, & risk assessment for breast cancer prevention. Cancer 109(12), 2635-2666. http://onlinelibrary.wiley.com/doi/10.1002/cncr.22653/abstract

17 Rayner, J. L., Enoch, R. R., & Fenton, S. E. (2005). Adverse Effects of Prenatal Exposure to Atrazine During a Critical Period of Mammary Gland Growth. Toxicological Sciences, 87 (1), 255-266. http://toxsci.oxfordjournals.org/cgi/content/short/87/1/255

18 Santella R. (1999) Immunologic methods for detection of carcinogen-DNA damage in humans. Cancer Epidemiology Biomarkers and Prevention 8,733–9. http://cebp.aacrjournals.org/content/8/9/733.full

19 Shimada, T. (2006). Xenobiotic-metabolizing enzymes involved in activation and detoxification of carcinogenic polycyclic aromatic hydrocarbons. Drug Metabolism Pharmokinesiology 21(4), 257-276. http://www.ncbi.nlm.nih.gov/pubmed/16946553

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Brain Cancer

1 Calderon-Garciduenas, L. et al. Brain Inflammation and Alzheimer’s-Like Pathology in Individuals Exposed to Severe Air Pollution. Toxicologic Pathology, Vol. 32, No. 6, 650-658 (2004) http://tpx.sagepub.com/cgi/content/abstract/32/6/650

1a Calderon-Garciduenas, L. et al. DNA Damage in Nasal and Brain Tissues of Canines Exposed to Air Pollutants Is Associated with Evidence of Chronic Brain Inflammation and Neurodegeneration Toxicologic Pathology, Vol. 31, No. 5, 524-538 (2003) http://tpx.sagepub.com/cgi/content/abstract/31/5/524

2 Singer, R. M. Neurotoxicity Guidebook, 1990. NY. Van Nostrand Reinhold.

3 Formaldehyde and Cancer Risk, National Cancer Institute, 11/20/2009 http://www.cancer.gov/cancertopics/factsheet/Risk/formaldehyde

4 Motohashi N, et al. Trichloroethylene. I. Carcinogenicity of trichloroethylene. Department of Medicinal Chemistry, Meiji Pharmaceutical University, Tokyo, Japan. In Vivo, 1999 May-Jun; 13(3):211-4. http://www.ncbi.nlm.nih.gov/pubmed/10459493

5 Black, K, Ljubimova, J. Brain Tumors and Air Pollution. Cedars Sinai Medical Center South Coast Air Quality Management District, Cal. USA 2005-2007

6 Sunyer J. 1,2,3 The neurological effects of air pollution in children. Eur Respir J 2008; 32:535-537 http://ersj.org.uk/cgi/content/full/32/3/535

7 Cordier S. *1, et al, Parental Exposure to Polycyclic Aromatic Hydrocarbons and the Risk of Childhood Brain Tumors: The SEARCH International Childhood Brain Tumor Study. Am J Epidemiol 2004; 159:1109-1116. http://aje.oxfordjournals.org/cgi/content/abstract/159/12/1109

8 Hannah S. Choi,1,2 et al. Residential Exposure to Toxics Release Inventory Chemicals during Pregnancy and Childhood Brain Cancer. Environ Health Perspect. 2006 July; 114(7): 1113?1118. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513318

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