5
Epidemiologic Studies: Compendium of New Publications
The continuing effort to evaluate and integrate epidemiologic studies pertinent to possible health effects of the chemicals of interest (COIs)—2,4-dichlorophenoxyacetic acid (2,4-D), 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and its contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 4-amino-3,5,6-trichloropicolinic acid (picloram), and dimethylarsinic acid (DMA or cacodylic acid)—has involved the review of thousands of publications over successive reports (the original retrospective report, eight updates prior to the current report, and three short reports on single issues, as delineated in the second and third paragraphs of Chapter 1). The search strategy used to identify these publications is described starting on the first page of Chapter 2, along with explanations of various refinements that have been employed since the initial volume in this series was prepared.
The first part of this chapter tabulates publications of primary epidemiologic research that appeared in the period from October 1, 2010 (the closing date for inclusion in Update 2010 [IOM, 2011]), through September 30, 2012, as a compendium of new information on human health outcomes considered by the present committee. In this chapter and later chapters, epidemiologic studies are organized into categories according to the populations being studied (Vietnam veterans, occupational populations other than Vietnam veterans, and nonoccupational populations affected by environmental exposures) or by study design (case-control). The various study designs (most important, cohort, case-control, and cross-sectional) have strengths and weaknesses that influence their potential to contribute evidence considered in the health-outcomes chapters.
The second part of this chapter provides design information on populations that are the subject of multiple references in this and earlier Veterans and
Agent Orange (VAO) reviews—including new studies of populations that have been studied previously and studies of new populations that had multiple health outcomes—to avoid repeating design information in multiple health-outcomes chapters. (Design information on studies of new populations that involve single health outcomes is provided in the various health-outcomes chapters.) For presentation of the background information, the study populations are arranged into categories on the basis of whether they are composed of Vietnam veterans, occupationally exposed workers, or environmentally exposed individuals or were assembled according to a case-control approach focused on particular health outcomes.
In addition to reviewing studies involving exposures to the specific COIs listed previously, this and earlier VAO committees have considered studies that examined compounds chemically related to the herbicides used in Vietnam, such as 2-(2-methyl-4-chlorophenoxy) propionic acid, hexachlorophene, and chlorophenols, particularly 2,4,5-trichlorophenol. Some publications did not indicate the specific herbicides to which study participants were exposed or the magnitude of exposure; those limitations were considered when the committee weighed the relevance of each publication, as detailed in Chapter 2. The committee also considers studies of exposure to polychlorinated biphenyls and other dioxin-like compounds (DLCs) informative if their results were reported in terms of TCDD toxic equivalents (TEQs) or concentrations of specific congeners of DLCs. Available details of exposure assessment and use of the resulting data in analyses are discussed in Chapter 3, which follows the same sequence to categorize study populations.
NEW EPIDEMIOLOGIC PUBLICATIONS
The new epidemiologic publications reviewed by the committee for this update are listed in Tables 5-1, 5-2, and 5-3. The conditions listed in the “Health Outcomes Reported” columns are indicative of the chapters in which the new publications are considered. Note, however, that studies assessing the occurrence of various cancers after exposure scenarios temporally comparable with exposure during military service are discussed in Chapter 8, which addresses cancer outcomes as applicable to the veterans themselves. Studies of childhood cancers in relation to parental exposure to the COIs are discussed in Chapter 10, which addresses possible adverse effects in veterans’ offspring. Cancer studies that consider only childhood exposure are not considered relevant to the committee’s charge.
Publications Reporting a Single Health Outcome in New Populations
New publications reporting a single health outcome in populations not studied previously are listed in Table 5-1, with an indication of the outcomes. De-
TABLE 5-1 Publications Reporting a Single Health Outcome in New Populations
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Studies of Vietnam Veterans | ||||
None | ||||
Occupational Studies | ||||
Kamel et al., 2012 | Case-control (nested) | Pesticides, herbicides, 2,4-D, 2,4,5-T, dicamba | ALS | AHS |
Environmental Studies | ||||
Buck Louis et al., 2011 | Cross-sectional | anti-estrogenic PCBs (correspond to dl PCBs) | Menstrual cycles | Women without reproductive problems |
Goncharov et al., 2011 | Cross-sectional | PCB subsets (mono-ortho TEQ, estrogenic) | Hypertension | Anniston (AL) Community Health Survey |
Kezios et al., 2012 | Pregnancy cohort | dl PCB 118 | Birth weight, gestational age | California Child Health and Development Studies, University of California, Berkeley |
Leijs et al., 2012 | Prospective cohort | Prenatal TEQs for dioxin/furans, dl PCBs | Sons’ thyroid metabolism at puberty | Mother–baby pairs from Netherlands (followup on cohort of Ilsen et al., 1996) |
Miyashita et al., 2011 | Cohort | Total dioxins, furans, dl PCBs (non-ortho and mono-ortho) in maternal blood (3rd trimester) | Immune function in offspring (infections [otitis media], allergies [asthma, eczema, food allergies]) | Hokkaido Study on Environment and Children’s Health Japanese mothers and infants examined at birth and at 18 months of age |
Nishijo et al., 2012 | Birth cohort | TEQs PCDD/Fs in breast milk 1 mo after birth | Infant growth (birth, 1 mo, 4 mo), neurodevelopment | Mother–infant pairs from contaminated area of Vietnam |
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Virtanen et al., 2012; Krysiak-Baltyn et al., 2012 | Case-control (nested) | TEQs for dioxins, furans, PCBs in placenta, individual results on comprehensive list of dl-PCBs; in breast milk | Congenital cryptorchidism; Seeking pattern of congeners distinguishing cases with cryptorchidism form controls [results of interest in Virtanen et al., 2012] | Danish-Finnish Prospective Cohort: boys examined at birth and 3 months of age |
Case-Control Studies | ||||
Band et al., 2011 | Case-control | 2,4-D, MCPA, dicamba | Prostate cancer | British Columbia farmers |
Bonefeld-Jorgensen et al., 2011 | Case-control | Sum dl PCBs, AHR-TEQs | Breast cancer | Inuit women from Greenland sampled 2000–2003 |
Cai et al., 2011 | Case-control | Dioxins, furans, all dl-PCBs, TEQ in peritoneal fluid and serum | Endometriosis | Japanese women undergoing diagnostic laparoscopy for infertility enrolled from October 2004 to March 2007 |
Gallagher et al., 2011 | Case-control | dl PCBs 118, 156, total dl PCBs in serum | Melanoma | Study participants were recruited using a population-based British Columbia Cancer Registry |
Lv et al., 2011 | Case-control | Occupational exposure to herbicides [marginal] | MDS | Shanghai, China |
Postuma et al., 2012 | Case-control | Occupational herbicide exposure, non-occupational only as specific as “pesticides” [marginal] | REM sleep behavior disorder (prognostic sign of PD and dementia) | Cases drawn from seven centers |
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Rollison et al., 2011 | Case-control | Pesticides, herbicides (case-control comparison shown for telomere length and then telomere length within MDS cases compared on basis of pesticide use) [marginal] | MDS (indirect evidence) | Newly diagnosed MDS cases in Florida |
Rugbjerg et al., 2011 | Case-control | Self-reported pesticide exposure (2,4-D & 2,4,5-T in “herbicides,” “pesticides with known neurotoxicity” classes) [marginal] | PD | British Columbia PD cases and controls |
Slater et al., 2011 | Case-control | Household chemicals (specificity to level of “herbicides”) [marginal] | Leukemia in infants | Infants diagnosed with acute leukemia at < 1 year of age at Children’s Oncology Group institutions in US and Canada |
Wong et al., 2010 | Case-control | Primarily job title, but also “herbicides” [marginal] | NHL | Newly diagnosed patients in Shanghai |
Zakerinia et al., 2012 | Case-control | Pesticides [for individual types]; Herbicides for all lymphomas | Lymphoid neoplasms (HL, NHL, multiple myeloma, T-cell) | Diagnoses at Nemazee Hospital, Shiraz, Iran |
NOTE: 2,4-D, 2,4-dichlorophenoxyacetic acid; 2,4,5-T, 2,4,5-trichlorophenoxyacetic acid; AHR, aryl hydrocarbon receptor; AHS, Agricultural Health Study; ALS, amyotrophic lateral sclerosis; dl, dioxin-like; HL, Hodgkin lymphoma; MCPA, 2-methyl-4-chlorophenoxyacetic acid; MDS, myelodysplastic syndrome; NHL, non-Hodgkin lymphoma; PCB, polychlorinated biphenyl; PCDD, polychlorinated dibenzo-p-dioxin; PCDF, polychlorinated dibenzofuran; REM, rapid eye movement; TEQ, total toxic equivalent.
scriptions and critiques of the designs of the studies are provided in the sections of the report that discuss the results related to particular health outcomes. The publications in this table are predominantly case-control studies, where the focus of the investigation is on a particular health outcome.
Publications Reporting Multiple Health Outcomes in New Populations
New publications reporting multiple health outcomes in populations not studied previously are listed in Table 5-2, with a list of outcomes that were investigated. Comprehensive discussions of the designs of the studies are presented in Chapter 6, organized according to the type of study population. The results, with comments related to their reliability or limitations, appear in the appropriate outcome-specific sections of Chapters 7–13.
New Publications on Previously Studied Populations
The new publications on previously studied populations are listed in Table 5-3. The new publications are reviewed in the context of the history of publications on the same populations to take into account the fact that they are not presenting entirely new evidence but rather enhancing a picture that has been emerging for many years.
A number of long-term studies of populations exposed to the COIs are of particular importance to the VAO project. The disease experiences of those populations are updated with the passage of time. Placing each new publication into its historical context helps the committee to combine the evidence from various publications appropriately and to take into consideration the interdependence of related publications. Such clusters of studies are useful in describing the course of a population’s response to an exposure, and joint consideration of an entire body of research on a population may yield insight into relationships with potential confounding factors.
Many groups potentially exposed to the COIs have been monitored periodically, including the cohorts of the International Agency for Research on Cancer (IARC) and the National Institute for Occupational Safety and Health (NIOSH); residents of Seveso; and Operation Ranch Hand and Army Chemical Corps personnel. For the sake of completeness, the discussions of specific health outcomes and the associated cumulative-results tables in Chapters 7–13 include references to publications discussed in previous VAO reports and to new publications. In drawing its conclusions, the committee combined the evidence in new publications and the evidence synthesized in the most recent update (Update 2010), taking into account the interdependence of related publications.
Individual researchers who belong to research consortia that are evaluating cohorts in large multicenter studies (such as the IARC and NIOSH cohort studies) sometimes publish reports based on the subsets of study participants that they themselves are monitoring. The VAO committees take into consideration all reports that have been published, including those based on entire cohorts and those based on subcohorts. In drawing its conclusions, the committee factored in both types of studies, taking into consideration the interdependence among related studies. In particular, some subcohort studies have access to information
TABLE 5-2 Publications on Multiple Health Outcomes in New Study Populations
Citation | Study Design | Exposure Measures(s) Having Results | Health Outcome(s) Reported | Study Population |
Studies of Vietnam Veterans | ||||
Kim JB et al., 2012 | Case-control | TCDD | HT, hyperlipidemia, clinical outcomes (rate and severity of major adverse coronary events) | Korean VV (50–70 yrs of age undergoing angiograms for acute coronary syndrome) |
Occupational Studies | ||||
None | ||||
Environmental Studies | ||||
Chang et al., 2011a | Cross-sectional | Serum PCDD/F TEQ | Insulin resistance | Taiwan, 1,449 nondiabetic residents around closed PCP factory |
Chang et al., 2011b | Cross-sectional | Serum PCDD/F TEQ | CVD | Taiwan, 914 residents without CVD around closed PCP factory |
Chang et al., 2012 | Cross-sectional | Serum PCDD/F TEQ, also consideration of diet as source | Blood chemistries [Indirect evidence—more like biologic plausibility] | Taiwan, workers from closed PCP factory vs residents vs general population |
Lee et al., 2010 | Nested case-control | dl-PCBs 105, 118, 156, 157, 167 in serum | Diabetes | CARDIA cohort |
Lee et al., 2011a | Nested case-control | dl-PCBs 105, 118, 156, 157, 167 in serum | Obesity, dyslipedemia, insulin resistance | CARDIA cohort participants; study subjects recruited at baseline in 1985–1986 and followed for 20 yrs |
Lee et al. 2011b | Cross-sectional and prospective | dl-PCBs 105, 118, 156, 157, 189 in serum | Diabetes | PIVUS (men and women analyzed together) |
Lee et al., 2012a | Cross-sectional and prospective | dl-PCBs 105, 118, 126, 156, 157, 169, 189 in serum | Abdominal obesity | PIVUS (men and women analyzed separately) |
Citation | Study Design | Exposure Measures(s) Having Results | Health Outcome(s) Reported | Study Population |
Lee et al., 2012b | Cross-sectional and prospective | dl-PCBs 105, 118, 126, 156, 157, 169, 189 in serum | stroke | PIVUS (men and women analyzed separately) |
Lind et al., 2012 | Cross-sectional and prospective | Circulating POPs (dl PCBs 105, 118, 126, 156, 157, 169, 189) | Atherosclerosis (carotid artery plaques, intima-media thickness, gray scale of median) | PIVUS study |
Rönn et al., 2011 | Cross-sectional, prospective | dl-PCBs 105, 118, 123, 169, 156, 157, 189 in serum | Fat mass, obesity | PIVUS study participants; Uppsala elderly |
Silverstone et al., 2012 | Cross-sectional | PCB subsets (mono-ortho TEQ, estrogenic) | Diabetes | Anniston (Alabama) Community Health Survey |
Stolevik et al., 2011 | Prospective cohort | Prenatal exposure, TEQs for all dioxins, furans, dl PCBs (estimated from mothers’ food frequency questionnaire) | Infection, eczema, wheeze | Birth cohort from Norwegian Mother and Child Cohort Study (MoBa) |
Case-Control Studies | ||||
Rocheleau et al., 2011 | Case-control | maternal occupational herbicides expo, 1 mo before conception, 1st trimester, or 2nd–3rd trimester | Hypospadias | National Birth Defects Prevention Study (NBDPS) |
NOTE: AO, Agent Orange; CARDIA, Coronary Artery Risk Development in Young Adults cohort; CVD, cardiovascular disease; dl, dioxin-like; HT, hypertension; NBDPS, National Birth Defects Prevention Study; PCB, polychlorinated biphenyl; PCDD, polychlorinated dibenzo-p-dioxin; PCDF, polychlorinated dibenzofuran; PCP, pentachlorophenol; PIVUS, Prospective Investigation of the Vasculature in Uppsala Seniors; POP, persistant organic pollutant; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; TEQ, total toxic equivalent; VV, Vietnam veteran.
TABLE 5-3 Publications on Previously Studied Populations
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Studies of Vietnam Veterans | ||||
None | ||||
Occupational Studies | ||||
Andreotti et al., 2010 | Cohort | Dicamba and BMI as factors for colon cancer [marginal] | Focus on BMI at enrollment and incidence of various cancers [not relevant] Colon cancer from interaction of dicamba and BMI | AHS (licensed pesticide applicators and spouses) |
Boers et al., 2012 | Cohort | Chlorophenoxy herbicides (plasma TCDD) | All cancers and specific (stomach, pancreas, trachea/ bronchus/lung, melanoma, genital, prostate, bladder, kidney, NHL, leukemia), and IHD | Subcohort of IARC cohort (Netherlands) [followup to 2006 like Boers et al. (2010)] |
Burns et al., 2011 | Cohort | 2,4-D | Cancer incidence (1985–2007) from all cancer and full spectrum individually | Subcohort of NIOSH (Dow Chemical, Midland, Michigan plant workers) |
Kenborg et al., 2012 | Cohort | Pesticide exposure mainly to herbicides (including phenoxys) [marginal] | Incidence PD and smoking-related cancers (lung, larynx, bladder) | Danish Union of Gardeners |
Koutros et al., 2010a | Cohort | Pesticides [2,4-D known to be among most frequently used herbicides] [marginal] | Cancer incidence (extended through 2006) from all cancers and full spectrum individually | AHS (licensed pesticide applicators: private, commercial and spouses) |
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Koutros et al., 2010b, 2011; Barry et al., 2011, 2012 | Nested case-control | 2,4,5-T; 2,4-D; 2,4,5-TP; dicamba | Prostate cancer incidence 1993–2003 [most complete dose response info in Koutros et al., 2011] | AHS (licensed pesticide applicators); interaction between pesticide use and SNPs (in metabolic DNA repair, and 8q24 genes) for prostate cancer risk |
Manuwald et al., 2012 | Cohort | Cumulative TCDD exposure estimated from tissue samples and job history | All cancers and full spectrum individually | German production workers at Hamburg plant (IARC) |
Ruder and Yiin, 2011 | Cohort | PCP (subgroups with and without exposure to TCDD in addition) | Mortality (to 2005) (full spectrum) | US PCP workers (NIOSH) |
Saberi Hosnijeh et al., 2011 | Cohort | 2,4-D, 2,4,5-T, 2,4,5-TCP, MCPA, MCPP | Humoral immunity (C-4, associated with NHL), atopic disease (asthma) | Subcohort of IARC (Dutch phenoxy herbicide workers) |
Saberi Hosnijeh et al., 2012 | Cohort | 2,4-D, 2,4,5-T, 2,4,5-TCP, MCPA, MCPP | Plasma cytokine concentrations (possible suppression of immunity) | Subcohort of IARC (Dutch phenoxy herbicide workers) |
Waggoner et al., 2011 | Cohort | Pesticides (2,4-D known to be among most frequently used herbicides) [marginal] | Mortality (1993–2007) (includes full spectrum of individual cancers; diabetes mellitus; and diseases of systems related to respiration, digestion, bone and connective tissue, heart and circulation) | AHS (licensed pesticide applicators and spouses) |
Environmental Studies | ||||
Cho et al., 2011 | Cross-sectional | DLCs (PCB 126, hpCDD, OCDD) | Bone mineral density, fat mass | NHANES (1999–2004) |
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Humblet et al., 2011 | Cohort | Dioxin, PCB concentrations in maternal blood (TEQs) | Pubertal onset | Mother–son pairs from Chapaevsk, Russia |
Jones et al., 2011 | Cross-sectional | Urinary arsenic | Hypertension | NHANES (2003–2008) |
Lambertino et al., 2011 | Cohort | Σdl PCBs | Uterine leiomyoma | Great Lakes Fish Consumption Study |
Mocarelli et al., 2011 | Cohort | Serum concentrations of TCDD | Sperm quality and reproductive hormones in offspring | Seveso; sons born (1977–1984) to dioxin-exposed mothers |
Su et al., 2012 | Cohort | TEQs for PCBs, PCDD/Fs | Reproductive development | Taiwanese Mother- and-Child Study; followup to 8 yrs of age |
Tsukimori et al., 2012b | Cohort | Dioxin, furan, and PCB TEQs in maternal blood extrapolated back to delivery | Birth weight (by sex of infant) | Yusho mothers and children |
Warner et al., 2011 | Cohort | Serum concentrations of TCDD | Breast cancer | SWHS (Seveso women 0–40 yrs old at time of accident; followup through 2008) |
Case-Control Studies | ||||
Hohenadel et al., 2011 | Case-control | Herbicides, phenoxys, 2,4-D alone and in combination with malathion | NHL | Cross-Canada Study of Pesticides and Health |
Karunanayake et al., 2012 | Case-control | ≥ 10 hr/yr pesticide expo (2,4-D, Mecoprop, MCPA, Diclofomethyl, and dicamba) | Hodgkin Lymphoma | Cross-Canada Study of Pesticides and Health |
Citation | Study Design | Exposure Measure(s) Having Results | Health Outcome(s) Reported | Study Population |
Pahwa et al., 2011 | Case-control | Pesticide use (results on all phenoxys, 2,4-D, Mecoprop, MCPA, Diclofop-methyl) | STS | Cross-Canada Study of Pesticides and Health |
Viel et al., 2011 | Case-control | TEQs for dioxins, furans, and dl PCBs | NHL | NHL cases using population-based cancer registry, living in vicinity of a solid-waste incinerator in France |
Yiin et al., 2012 | Case-control | Quantified pesticide exposure (phenoxys, 2,4-D, dicamba) | Gliomas | UMHS (pesticide applicators) |
NOTE: 2,4-D, 2,4-dichlorophenoxyacetic acid; 2,4,5-T, 2,4,5-trichlorophenoxyacetic acid; 2,4,5-TCP, 2,4,5-trichlorophenol; 2,4,5-TP, 2-(2,4,5-trichlorophenoxy) propionic acid; AHS, Agricultural Health Study; AML, acute myeloid leukemia; BMI, body mass index; CLL, chronic lymphocytic leukemia; CML, chronic myeloid leukemia; CNS, central nervous system; COI, chemical of interest; dl, dioxin-like; DLBCL, diffuse large B-cell lymphoma; DLC, dioxin-like compound; DNA, deoxyribonucleic acid; FL, follicular lymphoma; GI, gastrointestinal; HD, Hodgkin disease; hpCDD, heptachlorodibenzo-p-dioxin; IARC, International Agency for Research on Cancer; IHD, ischemic heart disease; MCL, mantle cell lymphoma; MCPA, 2-methyl-4-chlorophenoxyacetic acid; MM, multiple myeloma; MZL, marginal zone lymphoma; NHANES, National Health and Nutrition Examination Survey; NHL, non-Hodgkin lymphoma; NIOSH, National Institute of Occupational Safety and Health; OCDD, octachlorodibenzo-p-dioxin; PCB, polychlorinated biphenyl; PCDD, polychlorinated dibenzo-p-dioxin; PCDF, polychlorinated dibenzofuran; PCP, pentachlorophenol; SLL, small lymphocytic lymphoma; SNP, single-nucleotide polymorphism; STS, soft-tissue sarcoma; SWHS, Seveso Women’s Health Study; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; TEQ, total toxic equivalent; UMHS, Upper Midwest Health Study.
not available for the entire cohort, such as data on individual serum TCDD concentrations and personal information that can be used to adjust for confounders of concern. Furthermore, even when analyses based on an entire cohort would include data on a subcohort as a subset, reports on the subcohort might provide additional information on the consistency of the relationships among subcohorts, such as whether there are important subcohort-by-exposure interaction effects, when these issues were not considered in the full-cohort studies. As long as the structures of study populations are recognized, VAO committees have been less concerned about over-weighting unstable positive findings on small subgroups or giving “repeated consideration” to duplicative results than would be the case if a quantitative meta-analysis were being undertaken.
Many of the cohorts that have contributed to the cumulative findings of the VAO committees are no longer being followed; however, the cohorts’ histories are briefly recapitulated in the body of this report. Additional background information can be found in earlier reports in this series. It is notable that the literature search for this update identified only a single epidemiology study of physical (not mental) health outcomes and the COIs in Vietnam veterans (Kim et al., 2012); the Vietnam veterans were Korean servicemen and the comparisons involving presumed herbicide exposure were designed in such a fashion that the study provided no usable information on any health outcome.
Andreotti G, Hou L, Beane Freeman LE, Mahajan R, Koutros S, Coble J, Lubin J, Blair A, Hoppin JA, Alavanja M. 2010. Body mass index, agricultural pesticide use, and cancer incidence in the Agricultural Health Study cohort. Cancer Causes and Control 21(11):1759–1775.
Band PR, Abanto Z, Bert J, Lang B, Fang R, Gallagher RP, Le ND. 2011. Prostate cancer risk and exposure to pesticides in British Columbia farmers. Prostate 71(2):168–183.
Barry KH, Koutros S, Berndt SI, Andreotti G, Hoppin JA, Sandler DP, Burdette LA, Yeager M, Freeman LEB, Lubin JH, Ma X, Zheng T, Alavanja MCR. 2011. Genetic variation in base excision repair pathway genes, pesticide exposure, and prostate cancer risk. Environmental Health Perspectives 119(12):1726–1732.
Barry KH, Koutros S, Andreotti G, Sandler DP, Burdette LA, Yeager M, Beane Freeman LE, Lubin JH, Ma X, Zheng T, Alavanja MCR, Berndt SI. 2012. Genetic variation in nucleotide excision repair pathway genes, pesticide exposure and prostate cancer risk. Carcinogenesis 33(2):331–337.
Boers D, Portengen L, Bueno de Mesquita HB, Heederik D, Vermeulen R. 2010. Cause-specific mortality of Dutch chlorophenoxy herbicide manufacturing workers. Occupational and Environmental Medicine 67(1):24–31.
Boers D, Portengen L, Turner WE, Bueno de Mesquita HB, Heederik D, Vermeulen R. 2012. Plasma dioxin levels and cause-specific mortality in an occupational cohort of workers exposed to chlorophenoxy herbicides, chlorophenols and contaminants. Occupational and Environmental Medicine 69(2):113–118.
Bonefeld-Jorgensen EC, Long M, Bossi R, Ayotte P, Asmund G, Kruger T, Ghisari M, Mulvad G, Kern P, Nzulumiki P, Dewailly E. 2011. Perfluorinated compounds are related to breast cancer risk in Greenlandic Inuit: A case control study. Environmental Health: A Global Access Science Source 10:88.
Buck Louis GM, Rios LI, McLain A, Cooney MA, Kostyniak PJ, Sundaram R. 2011. Persistent organochlorine pollutants and menstrual cycle characteristics. Chemosphere 85(11):1742–1748.
Burns C, Bodner K, Swaen G, Collins J, Beard K, Lee M. 2011. Cancer incidence of 2,4-D production workers. International Journal of Environmental Research and Public Health 8(9):3579–3590.
Cai LY, Izumi S, Suzuki T, Goya K, Nakamura E, Sugiyama T, Kobayashi H. 2011. Dioxins in ascites and serum of women with endometriosis: A pilot study. Human Reproduction 26(1):117–126.
Chang JW, Chen HL, Su HJ, Liao PC, Guo HR, Lee CC. 2011a. Simultaneous exposure of non-diabetics to high levels of dioxins and mercury increases their risk of insulin resistance. Journal of Hazardous Materials 185(2-3):749–755.
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1Throughout this report, the same alphabetic indicator after year of publication is used consistently for a given reference when there are multiple citations by the same first author in a given year. The convention of assigning the alphabetic indicators in order of citation in a given chapter is not followed.
Chang JW, Chen HL, Chang CC, Su HJ, Liao PC, Lee CC. 2011b. Predicting the risk of cardiovascular disease in people exposed to moderate to high levels of dioxin. Journal of Hazardous Materials 198:317–322.
Chang JW, Chen HL, Su HJ, Liao PC, Lee CC. 2012. Biochemical study of retired pentachlorophenol workers with and without following dietary exposure to pcdd/fs. Chemosphere 88(7):813–819.
Cho MR, Shin JY, Hwang JH, Jacobs DR Jr, Kim SY, Lee DH. 2011. Associations of fat mass and lean mass with bone mineral density differ by levels of persistent organic pollutants: National Health and Nutrition Examination Survey 1999-2004. Chemosphere 82:1268–1276.
Gallagher RP, MacArthur AC, Lee TK, Weber JP, Leblanc A, Mark Elwood J, Borugian M, Abanto Z, Spinelli JJ. 2011. Plasma levels of polychlorinated biphenyls and risk of cutaneous malignant melanoma: A preliminary study. International Journal of Cancer 128(8):1872–1880.
Goncharov A, Pavuk M, Foushee HR, Carpenter DO. 2011. Blood pressure in relation to concentrations of PCB congeners and chlorinated pesticides. Environmental Health Perspectives 119(3):319–325.
Hohenadel K, Harris SA, McLaughlin JR, Spinelli JJ, Pahwa P, Dosman JA, Demers PA, Blair A. 2011. Exposure to multiple pesticides and risk of non-Hodgkin lymphoma in men from six Canadian provinces. International Journal of Environmental Research and Public Health 8(6):2320–2330.
Humblet O, Williams PL, Korrick SA, Sergeyev O, Emond C, Birnbaum LS, Burns JS, Altshul L, Patterson DG, Turner WE, Lee MM, Revich B, Hauser R. 2011. Dioxin and polychlorinated biphenyl concentrations in mother’s serum and the timing of pubertal onset in sons. Epidemiology 22(6):827–835.
Ilsen A, Briet JM, Koppe JG, Pluim HJ, Oosting J. 1996. Signs of enhanced neuromotor maturation in children due to perinatal load with background levels of dioxins. Follow-up until age 2 years and 7 months. Chemosphere 33(7):1317–1326.
IOM (Institute of Medicine). 2011. Veterans and Agent Orange: Update 2010. Washington, DC: The National Academies Press.
Jones MR, Tellez-Plaza M, Sharrett AR, Guallar E, Navas-Acien A. 2011. Urine Arsenic and hypertension in US adults. The 2003-2008 National Health and Nutrition Examination Survey. Epidemiology 22:153–161.
Kamel F, Umbach DM, Bedlack RS, Richards M, Watson M, Alavanja MCR, Blair A, Hoppin JA, Schmidt S, Sandler DP. 2012. Pesticide exposure and amyotrophic lateral sclerosis. NeuroToxicology 33(3):457–462.
Karunanayake CP, Spinelli JJ, McLaughlin JR, Dosman JA, Pahwa P, McDuffie HH. 2012. Hodgkin lymphoma and pesticides exposure in men: A Canadian case-control study. Journal of Agromedicine 17(1):30–39.
Kenborg L, Lassen CF, Lander F, Olsen JH. 2012. Parkinson’s disease among gardeners exposed to pesticides—A Danish cohort study. Scandinavian Journal of Work, Environment and Health 38(1):65–69.
Kezios KL, Liu X, Cirillio PM, Kalantzi OI, Wang Y, Petreas MX, Park JS, Bradwin G, Cohn BA, Factor-Litvak P. 2012. Prenatal polychlorinated biphenyl exposure is associated with decreased gestational length but not birth weight: Archived samples from the child health and development studies pregnancy cohort. Environmental Health: A Global Access Science Source 11(1):1—13.
Kim JB, Kang WY, Moon SG, Kim HJ, Kim KH, Kim YH, Hwang SH, Hwang SH, Kim W. 2012. Clinical outcome of veterans with acute coronary syndrome who had been exposed to Agent Orange. Chonnam Medical Journal 48(1):47–51.
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