Air Pollution and Breast Cancer

At a Glance

A hazardous air pollutant (HAP) or toxic air contaminant (TAC) is a chemical that causes cancer, reproductive harm, or other serious health effects resulting in disease and death. [1]

Few studies have examined breast cancer risk from air toxics among urban, diverse communities. A recent University of California Los Angeles (UCLA) study examining 16 hazardous chemicals in air pollution in the Los Angeles area and found that LA women face unsafe levels of exposure to hazardous air pollutants, and women of color bear a disproportionate breast cancer burden from exposure.

air toxic

Introduction

The air has many types of pollutants from a range of sources. In addition to the traffic and particulate pollutants in the air, hazardous chemicals are in the chemical mix. A hazardous air pollutant (HAP) or toxic air contaminant (TAC) is a chemical that causes cancer, reproductive harm, or other serious health effects resulting in disease and death. [1] These chemicals come from many sources including both traffic and non-traffic sources such as gas wells, hazardous waste sites, landfills, and polyvinyl chloride (PVC) manufacturing plants.

Few studies have examined breast cancer risk from air toxics among urban, diverse communities. Fenceline communities live near hazardous waste sites, gas wells, landfill sites, freeways, and ports and are affected by chemical emissions, noise, odors, and traffic. Fenceline communities in urban areas are particularly impacted by air pollutants including traffic, fossil fuel extraction, plastic and petroleum chemical emissions, landfills, waste incineration, and hazardous waste sites.

Research shows that the distribution of air pollution is disproportionately higher in communities of color compared to white communities. The NAACP report “Coal Blooded: Putting Profits Before People” found that 78% of all African Americans live within 30 miles of a coal-fired power plant.

The cumulative effects of being exposed to many air pollutants over many years can be particularly damaging to our health. Affected communities face many hazards from living near chemical emissions, but few breast cancer studies have examined breast cancer risk associated with exposure to hazardous air pollutants.

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What We’re Doing

Recent studies have demonstrated that traffic-related air pollutants can increase breast cancer risk. However, there are additional hazardous air pollution compounds that come from industrial emissions that we know less about. The scientific literature also lacks data on the impact of hazardous air pollutant exposure on ethnically diverse groups of women in urban environments as previous studies have oversampled white, rural areas.

A recent study conducted by University of California (UCLA) researchers examined 16 hazardous chemicals in air pollution in the Los Angeles area. [2] This study tracked breast cancer occurrence among Multiethnic Cohort participants from 1993-1996 through 2013 associated with air pollution data from the National-Scale Air Toxics Assessment 1998-2003 data.

Researchers used the levels of hazardous air pollutants that come from traffic, gas wells, fossil fuel power plants, manufacturing, landfill, and hazardous waste emissions. See Figure 1 for location of active gas wells in Los Angeles. By tracking exposure levels and breast cancer rates, researchers asked the question: Does the likelihood of breast cancer increase from exposure to hazardous air pollutants among women in Los Angeles?

Breast cancer attributable to chemical exposure in UCLA air toxics study
figure 2
air toxic

Figure 1. A map of active oil and gas wells in Los Angeles. Oil and gas well finder: https://maps.conservation.ca.gov/doggr/wellfinder/

Results found that among women from the Greater Los Angeles area (n=48,723), hazardous air pollutants significantly increased the likelihood of breast cancer. Researchers chose 16 hazardous chemicals that are endocrine disruptors or mammary gland carcinogens. Of 16 studied, 14 hazardous chemicals significantly increased the likelihood of getting breast cancer over the 20-year study period:

  • 6 of 11 hazardous chemicals came from traffic, gas wells, and fossil fuel power plant emissions (xylene exposure presented the highest breast cancer likelihood) (Figure 2)
  • 8 of 11 came from manufacturing, landfill, and hazardous waste emissions (vinyl acetate, vinyl chloride, ethylene dichloride, and 1,1,2,2 tetrachloroethane exposure presented the highest breast cancer likelihood) (Figure 2)
  • Increases in the likelihood of breast cancer from hazardous air pollutants were greatest for women of color (Figure 3).
figure 2

Figure 2. Percentage excess odds of getting breast cancer over a 20-year period [2] with chemicals on the y-axis and percentage increases in odds of getting breast cancer on the x-axis (n=48,723) Chemicals listed at the top of the graph are from traffic, gas wells, and fossil fuel power plants (xylenes, toluene, formaldehyde, ethylbenzene, benzene, and 1,2-butadiene) and those listed on the bottom of the graph are from plastics manufacturing, industrial, and waste emissions (vinyl acetate, 1,1,2,2-tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, acetaldehyde, naphthalene, and trichlorethylene).

Figure 3

Figure 3. Percentage Excess odds of getting breast cancer over a 20-year period [2] with chemicals on the y-axis and percentage increases in odds of getting breast cancer on the x-axis. Chemicals listed at the top of the graph are from traffic, gas wells, and fossil fuel power plants (xylenes, toluene, formaldehyde, ethylbenzene, and benzene) and those listed at the bottom of the graph are from plastics manufacturing, industrial, and waste emissions (vinyl acetate, 1,1,2,2-tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, and acetaldehyde). *Estimates for these chemicals among African Americans are not shown due to the lack of sufficient number of unexposed cases.

Learn About the Chemicals in This Study

All chemicals of concern included in this study are fossil fuel chemicals. Some are used in Chemicals of concern in this study:

  • Polyvinyl chemicals- vinyl chloride and ethylene dichloride are used to manufacture polyvinyl chloride (PVC) plastic and vinyl products. Vinyl chloride is a colorless gas released from landfills, sewage treatment plants, and hazardous waste sites. Vinyl chloride is genotoxic, inducing unscheduled DNA synthesis, increasing the frequency of sister chromatid exchange in rat and human cells, and increasing the frequency of chromosomal aberrations and micronucleus formation. Knowledge of the human carcinogenicity of vinyl chloride stems largely from several extensive occupational cohort studies of polyvinyl chloride manufacturing workers. Still, these studies included few women and knowledge about breast cancer impacts is lacking. Multiple animal studies have observed that inhalation of vinyl chloride increases the incidence of mammary tumors in mice, rats, and hamsters. [3] The US EPA classifies ethylene dichloride as a probable human carcinogen. [5-7]
  • Vinyl acetate is used for plastic and adhesives production in the preparation of polymers and copolymers (Daniels, 1983). The US EPA classifies ethylene dichloride as a probable human carcinogen. [5-7] Vinyl acetate has not been classified by the US EPA but has been designated as possibly carcinogenic to humans by the International Agency for Research on Cancer based on the following health effects:
    • (i) Vinyl acetate is rapidly transformed into acetaldehyde in human blood and animal tissues.
    • (ii) There is sufficient evidence in experimental animals for the carcinogenicity of acetaldehyde (IARC, 1987b). Both vinyl acetate and acetaldehyde induce nasal cancer in rats after administration by inhalation.
    • (iii) Vinyl acetate and acetaldehyde are genotoxic in human cells in vitro and in animals in vivo.
  • 1,1,2,2 tetrachloroethane is used as a common manufacturing byproduct in the process of catalytic chlorination. A study in experimental animals reported increased mammary gland fibroadenoma with 1,1,1,2-tetrachloroethane exposure. In humans, 1,1,1,2-tetrachloroethane accumulates in fat tissue; it appears genotoxic, but studies are limited. This toxicant is an understudied exposure; a 2014 IARC review did not identify any carcinogenicity studies in humans. [4]
  • Traffic-related chemicals- formaldehyde, benzene, ethylbenzene, toluenes, xylenes, and 1,2-butadiene come from power plant emissions, gas well emissions, and vehicle emissions (Figure 1). Together they are categorized as volatile organic compounds (VOCs). They come from natural sources, such as fire burning; however, human activity has been the main sources of prevalent VOCs in the air. Because of their biological structures and their easy volatilization, they easily enter our blood and lymph through inhalation, skin absorption, and orally through polluted water or food. Several studies point to their known association with various health and environmental consequences, including neurological impairment. Research indicates that even at low concentrations, VOCs can trigger a range of health issues, such as nausea, eye and throat irritation, the onset of asthma attacks, fatigue, dizziness, and cognitive impairment. Furthermore, persistent VOCs may also lead to cancer, pulmonary disease, skin problems, and immunological system disorders. [18-22]

Key Takeaways

Out of 181 toxic air pollutants that were considered for inclusion, UCLA researchers selected 57 agents identified as endocrine disruptors or suspected/established carcinogens. 16 of 57 were analyzed and 14 of the 16 significantly increased breast cancer likelihood. The remaining 41 endocrine disruptors and breast carcinogens (Figure 4) were not included in this analysis due to lack of unexposed cases. This means that there were not enough people with breast cancer who were not exposed to these chemicals to measure the impact of chemical exposure. This was particularly the case among African Americans, for whom estimates could not be made due to the lack of sufficient number of unexposed cases in case of three chemicals (1,1,2,2 tetrachloroethane, ethylene dichloride, and vinyl chloride). In other words, chemical exposure was so widespread for these three chemicals that among the study participants with breast cancer, there were too few African American participants who were unexposed to those chemicals to conduct statistical calculations of breast cancer likelihood. Based on the outcomes of this study, these remaining endocrine disruptors and breast carcinogens deserve further attention. 

figure 4

Figure 4. The 41 breast cancer carcinogens and endocrine disruptors were omitted from the UCLA Multiethnic Cohort study analysis. These chemicals weren’t included because there were insufficient numbers of women with breast cancer who were not exposed to these to calculate their risk. ​

Among the 48K women in this study, there were over 1500 breast cancer cases. To understand how many cancers in this study were attributed to chemical exposure, we calculated the population attributable fraction. We found that the chemicals of concern in this study are responsible for between 2-52% of breast cancer cases. Vinyl acetate, 1,1,2,2 tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, acetaldehyde and xylenes were responsible for the most breast cancer cases (between 19-52%) with the highest population attributable fractions seen for exposure to vinyl acetate (51.6%), 1,1,2,2-tetrachloroethane (44.6%), and ethylene dichloride (31%) (Figure 5). The highest population attributable fractions by race/ethnicity were: 

African Americans
• Among African Americans, the highest population attributable fractions were seen for exposure to vinyl acetate (71.8%), chloroform (64.1%), and acrolein (37.6%).

Japanese Americans
• Among Japanese Americans, the highest population attributable fractions were seen for exposure to 1,1,2,2-tetrachloroethane (63.5%), vinyl chloride (60.7%), and vinyl acetate (41.2%).

Latinos
• Among Latinos, the highest population attributable fractions were seen for exposure to vinyl acetate (47.9%), 1,1,2,2-tetrachloroethane (40%), and chloroform (31.3%).

Whites
• Among Whites, the highest population attributable fractions were seen for exposure to vinyl acetate (54.1%), ethylene dichloride (49.8%), and 1,1,2,2-tetrachloroethane (47%).

A key finding of this study is that the highest chemical exposure levels were not associated with the highest likelihood of getting breast cancer over the 20-year study period. Rather, the lowest levels of exposure from industrial hazardous air pollutants were associated with the greatest increases in likelihood of getting breast cancer. Figure 5 shows the low levels of exposure for vinyl acetate, 1,1,2,2 tetrachloroethane, and ethylene dichloride (EDC) on the left. On the right, we see the highly elevated likelihood of breast cancer associated with those same chemicals. This finding highlights the need to evaluate the health effects from low levels of exposure due to their ability to disrupt the endocrine system, which can lead to breast cancer.

Low Chemical Exposure High Risk

Figure 5. Exposure levels of hazardous air pollutants (left) compared to the percentage of breast cancer cases that would be removed if we were to remove exposure to that chemical (right). The x-axis on the left is the concentration of chemical exposure in ug/m3, and the x-axis on the right is the percentage attributable fraction of breast cancer by chemical. The y-axis shows chemicals from traffic, gas wells, and fossil fuel power plants (xylenes, toluene, formaldehyde, ethylbenzene, and benzene) on the top and from manufacturing and waste emissions (vinyl acetate, 1,1,2,2-tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, and acetaldehyde) on the bottom.

How did the UCLA Multiethnic Cohort study results compare to previous studies?

The most significant difference is that study participants herein were diverse and from an urban environment. [2] A previous study, the Sister Study, enrolled 85% White women with generally higher educational attainment than the Multiethnic cohort participants (53% of CA Multiethnic Cohort participants vs. 1.2% of Sister Study participants had less than a high school education). [9] As a result, Sister Study participants have higher socioeconomic status that and likely to reside in neighborhoods with lower industry pollutant levels. The California Teachers’ Study differed from the Multiethnic Cohort study both racially and geographically, as it included predominantly White women (89%) with oversampling in rural areas. Similarities between the UCLA study and the two previous studies are that they all reported increased breast cancer risk with vinyl chloride. The UCLA Multiethnic Cohort study had high traffic and industrial pollutant levels, as well as a higher pollution burden in neighborhoods with a high concentration of historically marginalized racial and ethnic groups which suggests that chemical exposure levels varied between the UCLA study described here [2] and the two previously published studies.

In summary, the analysis herein provides multiple lines of evidence that women in Los Angeles face unsafe levels of exposure to hazardous air pollutants, and that women of color bear a disproportionate breast cancer burden from exposure. Areas and individuals who’ve experienced historical environmental injustices due to the location of polluting industrial and waste disposal sources are at a disproportionately higher risk of breast cancer. Cumulative exposure (exposure to multiple chemicals) and aggregate exposure (exposures across multiple routes including oral, dermal, inhalation, and placental) to hazardous air pollutants remain a concern and present potent risk factors for breast cancer, particularly for vulnerable communities of color and fenceline communities. These findings show the importance of monitoring and mitigating hazardous air pollutants, even at low levels, to prevent breast cancer.

Read More About This Study

To fill the gap in understanding how hazardous air pollution exposures impact breast cancer risk, air pollution data from the National Air Toxics Assessment was linked to participant data from the Multiethnic Cohort, a large population-based group who live in California. Among the female participants (n=48,723), 40.4% described themselves as Hispanic or Latino, 33.4% African Americans, 14.9% white, 11.2% Japanese Americans, and 0.1% Native Hawaiians. 53% of the women had an education level of high school or lower. African American and Latino women were more likely to live in the lowest two quintiles of SES neighborhoods (66.2% and 58.8%, respectively) than white and Japanese American women (23.5% and 17.0%, respectively).

To ensure that researchers were studying the biological impacts of exposure to air pollution rather than differences due to sociodemographic and health factors, certain factors were controlled for in the analysis including age, race/ethnicity, education, anthropometrics, smoking, medical history, family history of cancer, medication history, work history, physical activity, reproductive history, and dietary data.

The Multiethnic Cohort Study found an increased likelihood of breast cancer with increased exposure to most air toxics, with strongest associations for vinyl acetate, 1,1,2,2 tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, acetaldehyde, and xylenes. This was the case despite relatively low exposure levels for vinyl acetate, 1,1,2,2 tetrachloroethane, ethylene dichloride, vinyl chloride (Figure 5).

Increased exposure to 1,1,2,2-tetrachloroethane resulted in a 322% elevated breast cancer risk (95% CI 218-460%). Increased exposure to ethylene dichloride resulted in 181% elevated breast cancer odds (95% CI 120-259%). Vinyl chloride increased odds by 127% (95% CI 81-185%). Traffic air pollution increased odds by 104% (95% there was increased likelihood of invasive breast cancer from higher exposure to 11 of 16 h CI 88-121%) for xylenes, 32% (95% CI of 24-41%) in the case of benzene, 20% (95% CI 13-28%) in the case of ethylbenzene, and 29% (95% CI 20-38%) for toluene, and 28% (95% CI 18-39%) in the case of formaldehyde (Figure 2).

The likelihood of breast cancer was even higher for communities of color. Hazardous manufacturing and waste chemicals represented the greatest threat to communities of color. For example, vinyl acetate increased the likelihood of getting breast cancer by 427% (95% CI 314-573%) and by 1030% (95% CI 636-1635%) among African Americans. For several of the chemicals, there were not enough breast cancer-positive participants with low levels of chemical exposure to assess the impacts of chemical exposure.

Previous studies on ambient air toxics and breast cancer have included various agents. The California Teachers’ Study, which also used NATA models (ASPEN) to estimate breast cancer risk, differed from this study both racially and geographically, as it includes largely White women (89%) recruited across California with oversampling in rural areas; thus, agents they could study only partially overlap with our study. Yet, both California studies found increases in breast cancer risk with vinyl chloride. The CTS only examined one traffic-related pollutant, benzene; comparable to our findings, the CTS reported increases in risk with traffic-related pollutants but only for ER-/PR- tumors. [10]

There was some heterogeneity of results by race and ethnicity. Differences observed by race and ethnicity likely reflect the varying pollution levels across neighborhoods of residence and not inherent differences by race and ethnicity in susceptibility to these air toxics. During the study period, African American participants lived primarily within the area bordered by Interstates 10, 405, 105, and 110 freeways (Inglewood) with high levels of traffic-related and other types of air pollution. [14-16]

In contrast, Japanese American participants lived in larger numbers in northeast LA (Monterey Park) and certain west side neighborhoods (Torrance and South Bay). Both White and Latino Multiethnic Cohort participants resided across the LA basin, but Whites were slightly more likely to live west and Latinos east of downtown Los Angeles. The variation in effect estimates may at least partially reflect varying concentrations of exposures in these distinct neighborhoods of residence.

In summary, these findings show the importance of local industry-related and traffic sources of air toxics in neighborhoods for breast cancer risk. Areas and individuals who’ve experienced historical environmental injustices due to the location of polluting sources are at disparate risk of breast cancer, according to these data.

A limitation of the study is that NATA models only provide air pollution estimates at the census tract level, as opposed to individual houses. Strengths of this study include the large cohort, the longitudinal timeframe, the prospective analysis, the ability to adjust for multiple confounders, and the detailed residential histories available for residents who lived in California during the study period.

Low exposure doesnt mean low risk

Policy Recommendations

Based on these and previous findings, women and communities of color are warranted greater protection from hazardous air pollutants including vinyl acetate, 1,1,2,2 tetrachloroethane, ethylene dichloride, vinyl chloride, acrolein, acetaldehyde, xylenes, benzene, toluene, formaldehyde, ethylbenzene, 1,3-butadiene, naphthalene, and trichloroethylene to lower their disproportionately high risk of breast cancer.

All policy and regulatory advances in the areas of hazardous chemical and plastic production reductions, fossil fuel emissions reductions, transit justice, transportation electrification, and anti-redlining will be beneficial to communities in that these actions lower exposure to both traffic-related and hazardous air pollutants. Areas of high priority that hold the potential to better protect our communities include:

  • Addressing exposure to chemicals used in PVC-related manufacturing (vinyl acetate, vinyl chloride, ethylene dichloride) and catalytic chlorination (1,1,2,2 tetrachloroethane). These exposures presented the most significant increases in statistical probability of getting breast cancer in this study. These chemicals should be reviewed for phaseout with urgency.
  • The scientific regulatory community needs to prioritize low-dose exposures to address the importance of exposure to breast cancer carcinogens and endocrine-disrupting chemicals in efforts to regulate chemicals aimed at preventing disease. The data herein document that the three chemicals that caused greatest increases in likelihood of breast cancer (vinyl acetate, 1,1,2,2 tetrachloroethane, vinyl chloride and ethylene dichloride) were at the lowest levels of exposure.

On a national and international scale, policy actions to limit/ban the production, use, and distribution of PVC will benefit fence line communities and communities of color, who are disproportionately exposed to hazardous chemicals. Vinyl chloride and ethylene dichloride are two chemicals needed to make PVC and are hazardous air pollutants that significantly increase breast cancer risk. Approximately 90% of the ethylene dichloride produced is dedicated to making vinyl chloride monomer, the chemical precursor to PVC. [17] Banning PVC plastic packaging in the US will have global benefits on the environment and cancer.

Additional Resources

Footnotes

[1] Hazardous air pollutants | US EPA. Accessed October 1, 2023. https://www.epa.gov/haps.

[2] Heck, J.E., He, D., Wing, S.E., Ritz, B., Carey, C.D., Yang, J., Stram, D.O., Le Marchand, L., Park, S.L., Cheng, I., Wo, A.H. Exposure to outdoor ambient air toxics and risk of breast cancer: The Multiethnic Cohort. J of International Journal of Hygiene and Environmental Health 259 (2024) 114362. https://www.sciencedirect.com/science/article/pii/S1438463924000439

[3] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Chemical Agents and Related Occupations. Lyon: International Agency for Research on Cancer; 2012.

[4] IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Trichloroethylene, tetrachloroethylene, and some other chlorinated agents. Lyon, France: International Agency for Research on Cancer, 2014.

[5] Naphthalene – U.S. environmental protection agency. 2016. Accessed October 1, 2023. https://www.epa.gov/sites/default/files/2016-09/documents/naphthalene.pdf.

[6] Ethylene dichloride (1,2-dichloroethane) – U.S. environmental protection agency. 2017. Accessed October 1, 2023. https://www.epa.gov/sites/production/files/2016-09/documents/ethylene-dichloride.pdf.

[7] Vinyl Acetate – U.S. Environmental Protection Agency. 2016. Accessed October 1, 2023. https://www.epa.gov/sites/default/files/2016-09/documents/vinyl-acetate.pdf.

[8] California EPA, Department of Toxic Substances Control, Human and Ecological Risk Office. Human Health Risk Assessment (HHRA) Note 3. June 2020 (Rev May 2022). Accessed October 1, 2023 https://dtsc.ca.gov/wp-content/uploads/sites/31/2022/02/HHRA-Note-3-June2020-Revised-May2022A.pdf.

[10] Sandler, Dale P., M. Elizabeth Hodgson, Sandra L. Deming-Halverson, Paula S. Juras, Aimee A. D’Aloisio, Lourdes M. Suarez, Cynthia A. Kleeberger, et al. “The Sister Study Cohort: Baseline Methods and Participant Characteristics.” Environmental Health Perspectives 125, no. 12 (2017). Accessed October 1, 2023. https://doi.org/10.1289/ehp1923.

[10] Garcia, Erika, Susan Hurley, David O Nelson, Andrew Hertz, and Peggy Reynolds. “Hazardous Air Pollutants and Breast Cancer Risk in California Teachers: A Cohort Study.” Environmental Health 14, no. 1 (2015). Accessed October 1, 2023. https://doi.org/10.1186/1476-069x-14-14.

[11] Niehoff, Nicole M., Marilie D. Gammon, Alexander P. Keil, Hazel B. Nichols, Lawrence S. Engel, Dale P. Sandler, and Alexandra J. White. “Airborne Mammary Carcinogens and Breast Cancer Risk in the Sister Study.” Environment International 130 (2019): 104897. Accessed October 1, 2023. https://doi.org/10.1016/j.envint.2019.06.007.

[12] Pastor, Manuel, James L. Sadd, and Rachel Morello-Frosch. “Waiting to Inhale: The Demographics of Toxic Air Release Facilities in 21st-Century California*.” Social Science Quarterly 85, no. 2 (2004): 420–440. Accessed October 1, 2023. https://doi.org/10.1111/j.0038-4941.2004.08502010.x.

[13] Niehoff, Nicole M., Mary Beth Terry, Deborah B. Bookwalter, Joel D. Kaufman, Katie M. O’Brien, Dale P. Sandler, and Alexandra J. White. “Air Pollution and Breast Cancer: An Examination of Modification by Underlying Familial Breast Cancer Risk.” Cancer Epidemiology, Biomarkers & Prevention 31, no. 2 (2021): 422–29. Accessed October 1, 2023. https://doi.org/10.1158/1055-9965.epi-21-1140.

[14] Cheng, Iona, Chiuchen Tseng, Jun Wu, Juan Yang, Shannon M. Conroy, Salma Shariff‐Marco, Lianfa Li, et al. “Association between Ambient Air Pollution and Breast Cancer Risk: The Multiethnic Cohort Study.” International Journal of Cancer 146, no. 3 (2019): 699–711. Accessed October 1, 2023. https://doi.org/10.1002/ijc.32308.

[15] Cushing, Lara, John Faust, Laura Meehan August, Rose Cendak, Walker Wieland, and George Alexeeff. “Racial/Ethnic Disparities in Cumulative Environmental Health Impacts in California: Evidence from a Statewide Environmental Justice Screening Tool (Calenviroscreen 1.1).” American Journal of Public Health 105, no. 11 (2015): 2341–48. https://doi.org/10.2105/ajph.2015.302643.

[16] “1,2-Dibromoethane.” National Center for Biotechnology Information. PubChem Compound Database, 2021. https://pubchem.ncbi.nlm.nih.gov/compound/1_2-Dibromoethane. National Center for Biotechnology Information; 2021.

[17] “EDC in PVC Production.” EDC in PVC production, 2010. https://www.engineeringspecifier.com/around-the-industry/edc-in-pvc-production.

[18] Garte, Seymour, Emanuela Taioli, Todor Popov, Claudia Bolognesi, Peter Farmer, and Franco Merlo. “Genetic Susceptibility to Benzene Toxicity in Humans.” Journal of Toxicology and Environmental Health, Part A 71, no. 22 (2008): 1482–89. Accessed October 3, 2023. https://doi.org/10.1080/15287390802349974.

[19] Abbate, C., C. Giorgianni, F. Muna, and R. Brecciaroli. “Neurotoxicity Induced by Exposure to Toluene.” International Archives of Occupational and Environmental Health 64, no. 6 (1993): 389–92. https://doi.org/10.1007/bf00517943.

[20] Yu, Chuck Wah, and Jeong Tai Kim. “Building Pathology, Investigation of Sick Buildings — VOC Emissions.” Indoor and Built Environment 19, no. 1 (2010): 30–39. https://doi.org/10.1177/1420326×09358799.

[21] Rolle-Kampczyk UE, Rehwagen M, Diez U, Richter M, Herbarth O and Borte M. “Passive smoking, excretion of metabolites, and health effects: Results of the Leipzig’s Allergy Risk Study (LARS).” Archives of Environmental Health 57, no 4 (2002): 326−31. DOI: https://doi.org/10.1080/00039890209601416.

[22] Montero-Montoya, Regina, Rocío López-Vargas, and Omar Arellano-Aguilar. “Volatile Organic Compounds in Air: Sources, Distribution, Exposure and Associated Illnesses in Children.” Annals of Global Health 84, no. 2 (2018): 225-238. Accessed October 3, 2023. https://doi.org/10.29024/aogh.910.

[23] Cheng, Iona, Juan Yang, Chiuchen Tseng, Jun Wu, Shannon M. Conroy, Salma Shariff-Marco, Scarlett Lin Gomez, et al. “Outdoor Ambient Air Pollution and Breast Cancer Survival among California Participants of the Multiethnic Cohort Study.” Environment International 161 (2022): 107088. Accessed October 1, 2023. https://doi.org/10.1016/j.envint.2022.107088

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