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1.
Occup Environ Med ; 68(6): 425-9, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21131604

RESUMO

OBJECTIVES: Numerous epidemiological studies of lung cancer among textile workers worldwide consistently indicate reduced risks related to cotton dust exposure, presumably due to endotoxin contamination. Our objective was to investigate associations with other exposures potentially related to lung cancer, including wool and synthetic fibre dusts, formaldehyde, silica, dyes and metals, that have only been studied to a limited extent in the textile industry. METHODS: We conducted a case-cohort study nested within a cohort of 267,400 women textile workers in Shanghai, China. We compared work assignments and exposure histories of 628 incident lung cancer cases, diagnosed during 1989-1998, with those of a reference subcohort of 3188 workers. We reconstructed exposures with a job-exposure matrix developed specifically for textile factories. Cox proportional hazards modelling was applied to estimate age/smoking-adjusted relative risks (hazard ratios) and risk gradients associated with job assignments and specific agents other than cotton dust and endotoxin. RESULTS: No associations were observed for lung cancer with wool, silk or synthetic fibre dusts, or with most other agents. However, increased risks, although statistically imprecise, were noted for ≥ 10 years' exposures to silica (adjusted HR 3.5, 95% CI 1.0 to 13) and ≥ 10 years' exposures to formaldehyde (adjusted HR 2.1, 95% CI 0.4 to 11). CONCLUSIONS: Exposures to silica and formaldehyde, although not widespread among the cohort, may have increased lung cancer risk. Silica is an established human lung carcinogen, whereas there is only weak prior evidence supporting an association with formaldehyde. Both exposures warrant consideration as potential lung carcinogens in textile manufacturing.


Assuntos
Neoplasias Pulmonares/etiologia , Doenças Profissionais/etiologia , Exposição Ocupacional/efeitos adversos , Indústria Têxtil , Idoso , Idoso de 80 Anos ou mais , China/epidemiologia , Fibra de Algodão , Poeira , Endotoxinas , Monitoramento Ambiental/métodos , Métodos Epidemiológicos , Monitoramento Epidemiológico , Feminino , Formaldeído/toxicidade , Humanos , Neoplasias Pulmonares/epidemiologia , Pessoa de Meia-Idade , Doenças Profissionais/epidemiologia , Exposição Ocupacional/análise , Dióxido de Silício/toxicidade , Fumar/efeitos adversos , Fumar/epidemiologia , Fatores de Tempo
2.
Occup Environ Med ; 66(3): 161-8, 2009 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-18805889

RESUMO

INTRODUCTION: To investigate possible associations between miscarriage and occupational exposures in the Shanghai textile industry. METHODS: A retrospective cohort study of miscarriages among 1752 women in the Shanghai textile industry was conducted. Reproductive history was self-reported by women and occupational work histories were collected from factory personnel records. Occupational exposures were assigned by linking work history information to an industry-specific job-exposure matrix informed by factory-specific textile process information and industrial hygiene assessments. Estimates of cotton dust and endotoxin exposure were also assigned. Odds ratios (OR) and 95% CI were estimated by multivariate logistic regression, with adjustment for age at pregnancy, educational level, smoking status of the woman and her spouse, use of alcohol, and woman's year of birth. RESULTS: An elevation in risk of a spontaneously aborted first pregnancy was associated with exposure to synthetic fibres (OR 1.89, 95% CI 1.20 to 3.00) and mixed synthetic and natural fibres (OR 3.31, 95% CI 1.30 to 8.42). No increased risks were observed for women working with solvents, nor were significant associations observed with quantitative cotton dust or endotoxin exposures. Associations were robust and similar when all pregnancies in a woman's reproductive history were considered. CONCLUSIONS: Occupational exposure to synthetic fibres may cause miscarriages, and this possibility should be the subject of further investigation.


Assuntos
Aborto Espontâneo/etiologia , Poluentes Ocupacionais do Ar/toxicidade , Poeira , Doenças Profissionais/etiologia , Indústria Têxtil , Aborto Espontâneo/induzido quimicamente , Adulto , Idoso , China , Estudos de Coortes , Fibra de Algodão , Endotoxinas/toxicidade , Feminino , Humanos , Pessoa de Meia-Idade , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional , Razão de Chances , Gravidez , Medição de Risco/métodos
3.
Occup Environ Med ; 63(12): 788-93, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-16847032

RESUMO

OBJECTIVES: To investigate whether occupational exposures to dusts and chemicals in the Shanghai textile industry are associated with risk of pancreatic cancer. METHODS: A case cohort study nested in a cohort of 267,400 female textile workers in Shanghai, China was conducted among 180 incident pancreatic cancer cases and an age stratified randomly selected comparison subcohort (n = 3188). A complete occupational history of work in the textile industry was obtained for each woman, and was linked to a job exposure matrix developed for the textile industry to estimate exposures to specific dusts and chemicals. Cumulative exposures to cotton dust and endotoxin were reconstructed from historical and contemporaneous measurements. RESULTS: After adjusting for smoking status, a trend of decreasing risk of pancreatic cancer was observed for increasing cumulative exposures to cotton dust and endotoxin with a lag of 20 years. The hazard ratios for women cumulatively exposed to >143.4 mg/m3 x years of cotton dust and >3530.6 EU/m3 x years of endotoxin were 0.6 (95% CI 0.3 to 0.9) and 0.5 (95% CI 0.3 to 0.9), respectively, compared to unexposed women. There was little evidence that exposures to other textile dusts and chemicals were associated with risk of pancreatic cancer. CONCLUSIONS: Occupational exposure to cotton dust and endotoxin in the textile industry may have reduced risks of pancreatic cancer in this cohort. These associations should be replicated by others before making a firm conclusion of their possible effects on pancreatic cancer.


Assuntos
Doenças Profissionais/etiologia , Neoplasias Pancreáticas/etiologia , Indústria Têxtil/estatística & dados numéricos , Adulto , Idoso , China/epidemiologia , Poeira , Endotoxinas/análise , Endotoxinas/toxicidade , Monitoramento Ambiental/métodos , Métodos Epidemiológicos , Monitoramento Epidemiológico , Feminino , Humanos , Pessoa de Meia-Idade , Doenças Profissionais/epidemiologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Neoplasias Pancreáticas/epidemiologia
4.
Int Arch Occup Environ Health ; 79(3): 251-8, 2006 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-16220287

RESUMO

OBJECTIVES: Thyroid cancer risk has been previously associated with increased age at first pregnancy and history of miscarriage. Occupational risk factors for thyroid cancer, with the exception of radioactive iodine, have not been well investigated. We conducted a case-cohort study nested in a cohort of 267,400 female textile workers in Shanghai, China, who had been followed for cancer incidence during 1989-1998. METHODS: The analysis included 130 incident thyroid cases and 3,187 subcohort non-cases. Reproductive history was determined by questionnaire at baseline. Historical exposures were reconstructed from work history and information on factory processes and exposures. Cox proportional hazards analysis was performed to estimate hazard ratios (HR) for reproductive factors and occupational exposures. RESULTS: Associations were observed between thyroid cancer and employment in jobs with 10 or more years of benzene exposure (HR 6.43, 95% CI: 1.08, 38) and formaldehyde exposure (HR 8.33, 95% CI: 1.16, 60). Administration workers also had an increased risk (HR 1.56, 95% CI: 1.08, 2.25). No associations between examined reproductive factors and thyroid cancer were observed in this study. CONCLUSIONS: Despite statistically imprecise risk estimates, the findings suggest potential associations with some occupational chemical exposures in this cohort of textile workers.


Assuntos
Poluentes Ocupacionais do Ar/efeitos adversos , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional/efeitos adversos , História Reprodutiva , Indústria Têxtil , Neoplasias da Glândula Tireoide/induzido quimicamente , Adulto , Idoso , Consumo de Bebidas Alcoólicas , China/epidemiologia , Feminino , Humanos , Estado Civil , Pessoa de Meia-Idade , Doenças Profissionais/epidemiologia , Medição de Risco , Fumar , Neoplasias da Glândula Tireoide/epidemiologia
5.
Occup Environ Med ; 63(1): 39-44, 2006 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-16361404

RESUMO

AIMS: To investigate whether occupational exposure to dusts and chemicals in the Chinese textile industry are associated with risk of nasopharyngeal cancer. METHODS: Sixty seven nasopharyngeal carcinoma (NPC) cases identified during 1989-98 and a random sample (n = 3188) of women were included in a case cohort study nested in a cohort of 267,400 women textile workers in Shanghai, China. A complete occupational history of work in the textile industry was obtained for each woman. A job exposure matrix developed by experienced industrial hygienists was used to assess exposures to specific dusts and chemicals. RESULTS: Risk of NPC is associated with cumulative exposure to cotton dust. The hazard ratio for women cumulatively exposed to >143.4 mg/m3 x years of cotton dust was 3.6 (95% CI 1.8 to 7.2) compared with unexposed women. Trends of increasing risk were also found with increasing duration of exposure to acids and caustics (p = 0.05), and with years worked in dyeing processes (p = 0.06). Women who worked at least 10 years in dyeing processes had a 3.6-fold excess risk of NPC (95% CI 1.0 to 12.1). CONCLUSIONS: Occupational exposure to cotton dust, acids, and caustics, and work in dyeing and printing jobs in the textile industry may have increased risk of NPC in this cohort.


Assuntos
Neoplasias Nasofaríngeas/etiologia , Doenças Profissionais/etiologia , Indústria Têxtil , Adulto , Distribuição por Idade , Idoso , China/epidemiologia , Poeira/análise , Endotoxinas/análise , Endotoxinas/toxicidade , Monitoramento Ambiental/métodos , Monitoramento Epidemiológico , Feminino , Humanos , Pessoa de Meia-Idade , Neoplasias Nasofaríngeas/epidemiologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Modelos de Riscos Proporcionais , Fatores de Risco
6.
Cancer Causes Control ; 16(10): 1177-88, 2005 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-16215868

RESUMO

Previous studies have suggested increased risks of colorectal cancers among textile industry workers, potentially related to synthetic fibers. To investigate risks of colon and rectum cancers in relation to these and other textile industry exposures, we conducted a case-cohort study nested within a cohort study of female employees from the Shanghai Textile Industry Bureau (STIB). Cox proportional hazard regression modeling was used to estimate hazard ratios (HR) for colon and rectum cancers associated with duration of employment (e.g., 0, >0 to <10, 10 to <20 years, > or =20 years) in various jobs classified according to process type and exposures to specific agents. Our findings indicate that certain long term exposures may pose increased risk of colorectal cancers, especially dyes and dye intermediates with colon cancer (> or =20 years exposure versus never, HR=3.9; 95% CI: 1.4-10.6), and maintenance occupation (HR = 2.3; 95% CI: 1.0-5.7) and metals exposure (HR = 2.0; 95% CI: 1.1-3.6) with rectum cancer. A decreased risk of rectum cancer was associated with exposure to natural fibers such as cotton (HR = 0.7; 95% CI: 0.5-0.9), and a trend of decreasing rectum cancer incidence was observed by category of cumulative quantitative cotton dust or endotoxin exposures, when exposures were lagged by 20 years.


Assuntos
Neoplasias do Colo/epidemiologia , Doenças Profissionais/epidemiologia , Exposição Ocupacional/efeitos adversos , Neoplasias Retais/epidemiologia , Indústria Têxtil , Adulto , Idoso , China/epidemiologia , Estudos de Coortes , Corantes/efeitos adversos , Feminino , Humanos , Incidência , Metais/efeitos adversos , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais
7.
Cancer Res ; 61(23): 8459-64, 2001 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-11731428

RESUMO

In vitro and animal models suggest that the herpes simplex virus 1 (HSV1) may contribute to the development of oropharyngeal squamous cell carcinoma (OSCC). To determine whether the risk of OSCC is related to infection with HSV1 in humans, we recruited 260 patients from 18 to 65 years old who were newly diagnosed with OSCC between 1990-1995 while residing in three western Washington State counties. For comparison, we recruited at random 445 controls frequency matched to cases on age and sex. Participants completed in-person interviews and provided serum samples that were tested for antibody response to HSV1. After adjusting for sex, cigarette smoking, alcohol consumption, age, and income, HSV1 antibody positivity was associated with a slightly increased risk of OSCC [adjusted odds ratio (OR), 1.3; 95% confidence interval (CI), 0.9-2.0]. The adjusted association between HSV1 antibody positivity and OSCC risk among those who were current cigarette smokers (OR, 4.2; CI, 2.4-7.1) was stronger than would be predicted based on the additive combination of smoking alone (OR, 2.3; CI, 1.2-4.2) and HSV1 seropositivity alone (OR, 1.0; CI, 0.6-1.7). There was suggestive evidence that the association between HSV1 infection and OSCC was similarly modified by evidence of HPV infection but no evidence of effect modification with alcohol consumption. This population-based study suggests that HSV1 may enhance the development of OSCC in individuals who are already at increased risk of the disease because of cigarette smoking or HPV infection.


Assuntos
Herpes Simples/complicações , Herpesvirus Humano 1 , Neoplasias Orofaríngeas/virologia , Adolescente , Adulto , Idoso , Anticorpos Antivirais/sangue , Estudos de Casos e Controles , Feminino , Herpes Simples/sangue , Herpes Simples/epidemiologia , Herpesvirus Humano 1/imunologia , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Orofaríngeas/sangue , Neoplasias Orofaríngeas/epidemiologia , Fatores de Risco
8.
Carcinogenesis ; 22(12): 1993-9, 2001 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-11751430

RESUMO

The risk of squamous cell cancers of the oral cavity (OSCC) is strongly related to the use of tobacco and alcohol. N-Acetyl transferases 1 and 2 (NAT2) metabolize aryl- and heterocyclic amines that are present in tobacco smoke. NAT2 slow acetylator phenotype or genotype is related to reduced ability to detoxify these xenobiotics that are carcinogenic in tissues in which smoking-related cancers develop (e.g. bladder). We studied the association between the deduced NAT2 acetylator phenotypes and OSCC risk in a population-based study of 341 cases and 552 controls. In-person interviews provided information on tobacco use and alcohol consumption. Nucleotide substitutions at position 191, 341, 590, 803 and 857 were determined by a combination of oligonucleotide ligation assays and PCR/RFLP assays. There was no overall association between acetylator status with OSCC risk; the odds ratios for slow and intermediate acetylators, as compared with the rapid acetylators, were 1.2 (95% CI 0.7-2.2) and 1.1 (95% CI 0.6-2.0), respectively. The percent increase in risk of OSCC per pack-year cigarette smoking was similar among slow acetylators (3.0%, 95% CI 2.1-4.0) and the combined intermediate and rapid acetylators (3.5%, 95% CI 2.4-5.0). In contrast, the risk of OSCC per weekly alcoholic drink was stronger among the combined rapid and intermediate acetylators (3.3%, 95% CI 1.8-4.9) compared with slow acetylators (1.6%, 95% CI 0.6-2.7) (interaction P = 0.055). These data raise the possibility that NAT2 may be involved in the activation of one or more pro-carcinogens associated with alcohol consumption.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Arilamina N-Acetiltransferase/genética , Predisposição Genética para Doença/genética , Neoplasias Bucais/etiologia , Neoplasias de Células Escamosas/etiologia , Polimorfismo Genético/genética , Fumar/efeitos adversos , Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Neoplasias Bucais/genética , Neoplasias de Células Escamosas/genética , Razão de Chances , Fatores de Risco , Alcatrões/efeitos adversos
9.
Cancer Epidemiol Biomarkers Prev ; 10(11): 1137-44, 2001 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-11700261

RESUMO

Heavy alcohol consumption, particularly in combination with cigarette smoking, increases the risk of oral squamous cell carcinoma (OSCC). Alcohol dehydrogenase 3 (ADH3) converts ethanol to acetaldehyde, which is a suspected oral carcinogen. The ADH3*1 allele is associated with increased conversion of ethanol to acetaldehyde, but whether the risk of OSCC is increased among ADH3*1 carriers, or whether the risk of OSCC attributable to alcohol consumption is modified by ADH3 genotype is unclear from previous studies. We examined the association between ADH3 genotypes, alcohol consumption, and OSCC risk in a population-based study of 333 cases and 541 controls from the state of Washington. The distribution of ADH3 genotypes was similar among cases and controls: ADH3*1/*1: 32.7% cases, 36.5% controls; ADH3*1/*2: 49.0% cases, 43.1% controls: ADH3*2/*2: 18.3% cases, 20.3% controls. The age-, sex-, and race-adjusted odds ratios (OR), relative to ADH3*2/*2 carriers, were as follows: ADH*1/*1: OR, 1.0 [95% confidence interval (CI) = 0.7, 1.5]; and ADH3*1/*2: OR, 1.3 (95% CI = 1.0, 1.8). We modeled the risk of OSCC associated with alcohol consumption as modified by ADH3 genotype adjusting for age, sex, race, and cigarette smoking. Among ADH3*2 homozygotes, the risk of OSCC increased 5.3% (2.1-8.5%) with each additional alcoholic drink/week, compared with 2.5% (1.5-2.6%) and 1.2% (0.0-2.4%) among persons carrying the ADH3*1/*2 and ADH3*1/*1 genotypes, respectively. These data suggest that the ADH3*2 allele confers increased susceptibility to the effect of alcohol on OSCC risk in our population.


Assuntos
Consumo de Bebidas Alcoólicas/metabolismo , Aldeído Oxirredutases/genética , Carcinoma de Células Escamosas/epidemiologia , Neoplasias Bucais/epidemiologia , Adulto , Carcinoma de Células Escamosas/genética , Estudos de Casos e Controles , Genótipo , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Neoplasias Bucais/genética , Fatores de Risco
10.
J Natl Cancer Inst ; 90(21): 1626-36, 1998 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-9811312

RESUMO

BACKGROUND: Experimental models and analyses of human tumors suggest that oncogenic, sexually transmittable human papillomaviruses (HPVs) are etiologic factors in the development of oral squamous cell carcinoma (SCC). We conducted a population-based, case-control study to determine whether the risk of this cancer is related to HPV infection and sexual history factors. METHODS: Case subjects (n = 284) were 18-65-year-old residents of three counties in western Washington State who were newly diagnosed with oral SCC from 1990 through 1995. Control subjects (n = 477) similar in age and sex were selected from the general population. Serum samples were tested for HPV type 16 capsid antibodies. Exfoliated oral tissue collected from case and control subjects and tumor tissue from case subjects were tested for HPV DNA. Odds ratios (ORs) were calculated after adjusting for age, sex, cigarette smoking, and alcohol consumption. RESULTS: Among males only, oral SCC risk increased with self-reported decreasing age at first intercourse, increasing number of sex partners, and a history of genital warts. Approximately 26% of the tumors in case subjects contained HPV DNA; 16.5% of the tumors contained HPV type 16 DNA. The prevalence of oncogenic HPV types in exfoliated oral tissue was similar in case and control subjects. The ORs for HPV type 16 capsid seropositivity were 2.3 (95% confidence interval [CI] = 1.6-3.3) for all oral SCCs and 6.8 (95% CI = 3.0-15.2) for oral SCCs containing HPV type 16 DNA. The joint association of cigarette smoking and HPV type 16 capsid seropositivity with oral SCC (OR = 8.5; 95% CI = 5.1-14.4) was stronger than predicted from the sum of individual associations with current smoking (OR = 3.2; 95% CI = 2.0-5.2) and seropositivity (OR = 1.7; 95% CI = 1.1-2.6). CONCLUSIONS: HPV type 16 infection may contribute to the development of a small proportion of oral SCCs in this population, most likely in combination with cigarette smoking.


Assuntos
Carcinoma de Células Escamosas/virologia , Neoplasias Bucais/virologia , Papillomaviridae , Infecções por Papillomavirus/complicações , Comportamento Sexual , Infecções Tumorais por Vírus/complicações , Adulto , Consumo de Bebidas Alcoólicas/efeitos adversos , Estudos de Casos e Controles , DNA de Neoplasias/análise , DNA Viral/análise , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Papillomaviridae/genética , Infecções por Papillomavirus/virologia , Prevalência , Risco , Fatores de Risco , Fumar/efeitos adversos , Infecções Tumorais por Vírus/virologia , Washington
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