Lung cancer has become a global problem, from a rare disease to an emerging public health issue. The current data of GLOBOCAN 2018, indicates that this disease has recorded highest mortality among all types of cancer. The etiological factors of lung cancer have become more multiplex because of increasing industrialization and environmental pollution around the world, especially in India. There is a rise in incidence of lung cancer among non-smokers and this can be attributed to environmental and occupational exposure to various kinds of hazardous substances. Target mutations are high in Lung cancer among non-smokers when compared to smokers. Some developed countries have guidelines and policies for prevention and control of risk factors focusing on these issues. Intervention aiming for primary prevention can be an important and cost-effective tool in developing countries to deal with increasing incidence of lung cancer. There is a need to define high risk group among non-smokers after taking into account environmental and occupational determinants as important risk factors. Research on etiology of lung cancer and prevention provides evidence to work on global incidence and prevalence of lung cancer, and for designing cost effective lung cancer prevention strategies. Research in the area of lung cancer prevention should be considered to recognize the areas where action is required to prevent environment and occupation related lung cancer. The government and occupational health and safety organizations have taken many steps in the last few years that can help to protect workers from these exposures. But the dangers are still there, so there is a need to do more to limit these exposures around workplace. This whole situation guides us to advocate population-based intervention along with policy implementation.

Liver cancer is the second leading worldwide cause of cancer‑associated mortalities. Hepatocellular carcinoma, which accounts for the majority of liver tumors, ranks fifth among types of human cancer. Well‑established risk factors for liver cancer include the hepatitis B and C viruses, aflatoxins, alcohol consumption, and oral contraceptives. Tobacco smoking, androgenic steroids, and diabetes mellitus are suspected risk factors. Current knowledge regarding non‑infective occupational risk factors for liver cancer is inconclusive. The relevance of liver disorders to occupational medicine lies in the fact that the majority of chemicals are metabolized in the liver, and toxic metabolites generated via metabolism are the predominant cause of liver damage. However, their non‑specific clinical manifestations that are similar in a number of liver diseases make diagnosis difficult. Furthermore, concomitant conditions, such as viral hepatitis and alcohol or drug abuse, may mask liver disorders that result from occupational hepatotoxic agents and block the demonstration of an occupational cause. The identification of environmental agents that result in human cancer is a long and often difficult process. The purpose of the present review is to summarize current knowledge regarding the association of non‑infective occupational risk exposure and HCC, to encourage further research and draw attention to this global occupational public health problem.

Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The main risk factors for HCC are alcoholism, hepatitis B virus, hepatitis C virus, nonalcoholic steatohepatitis, obesity, type 2 diabetes, cirrhosis, aflatoxin, hemochromatosis, Wilson's disease and hemophilia. Occupational exposure to chemicals is another risk factor for HCC. Often the relationship between occupational risk and HCC is unclear and the reports are fragmented and inconsistent. This review aims to summarize the current knowledge regarding the association of infective and non-infective occupational risk exposure and HCC in order to encourage further research and draw attention to this global occupational public health problem.

Given the large number of workers in the construction industry, it is important to derive accurate and valid estimates of cancer risk, and in particular lung cancer risk. In most previous studies, risks among construction workers were compared with general populations including blue and white collar workers. The main objectives of this study were to assess whether construction workers experience excess lung cancer risk, and whether exposure to selected construction industry exposures carries excess risks. We wished to address these objectives within the sub-population of blue collar workers.

Two case-control studies were conducted in Montreal. Combined, they included 1593 lung cancer cases and 1427 controls, of whom 1304 cases and 1081 controls had been blue collar workers. Detailed lifetime job histories were obtained and translated by experts into histories of exposure to chemical agents. The two key analyses were to estimate odds ratio (OR) estimates of lung cancer risk: a) for all blue-collar construction workers compared with other blue-collar workers, and b) for construction workers exposed to each of 20 exposure agents found in the construction industry compared with construction workers unexposed to those agents. All analyses were conducted using unconditional logistic regression adjusted for socio-demographic factors and smoking history.

The OR for all construction workers combined was 1.11 (95 % CI: 0.90-1.38), based on 381 blue collar construction workers. Analyses of specific exposures were hampered by small numbers and imprecise estimates. While none of 20 occupational agents examined was significantly associated with lung cancer, the following agents manifested non-significantly elevated ORs: asbestos, silica, Portland cement, soil dust, calcium oxide and calcium sulfate.

Compared with other blue collar workers, there was only a slight increased risk of lung cancer for subjects who ever held an occupation in the construction industry. The analyses of agents within the construction industry produced imprecise estimates of risk, but nevertheless pointed to some plausible associations. Excess risks for asbestos and silica were in line with previous knowledge. The possible excess risks with the other inorganic dusts require further corroboration.

Much evidence show that over-expression of epidermal growth factor receptor (EGFR) plays an important role in regulating carcinogenesis. Genetic variations in 3' untranslated region (3'UTR) of gene have been reported to affect gene expression by interfering with microRNAs (miRNAs), which are thought to function as either tumour suppressors or oncogenes by binding to their target mRNA. In this study, we investigated the association between the EGFR 3'UTR 774T>C polymorphism and bladder cancer risk. We used the TaqMan technology to genotype this genetic variant in a hospital-based case-control study of 908 bladder cancer patients and 1239 controls in a Chinese population. We found that the 774CC genotype was associated with a statistically significantly increased risk of bladder cancer [adjusted odds ratio = 1.29, 95% confidence interval = 1.05-1.58], compared with the 774TT/TC genotype, and this increased risk was more pronounced among subgroups of age > 65 years, non-smokers and patients' tumour invasive stage. Furthermore, luciferase assays in T24 cell showed that EGFR 3'UTR 774 T to C substitution could increase the expression of EGFR, which was consistent with the association study finding. Additionally, we also provide evidence that 774T>C polymorphism increasing EGFR expression was not regulated by hsa-miR-214 binding. These findings suggested that EGFR 3'UTR 774T>C polymorphism may contribute to susceptibility to bladder cancer.

We used data from a large, population-based case-control study in Maine, New Hampshire, and Vermont to examine relationships between occupation, industry and bladder cancer risk.

Lifetime occupational histories were obtained by personal interview from 1158 patients newly diagnosed with urothelial carcinoma of the bladder in 2001-2004, and from 1402 population controls. Unconditional logistic regression was used to calculate ORs and 95% CIs, adjusted for demographic factors, smoking and employment in other high-risk occupations.

Male precision metalworkers and metalworking/plasticworking machine operators had significantly elevated risks and significant trends in risk with duration of employment (precision metalworkers: OR 2.2, 95% CI 1.4 to 3.4, p(trend) = 0.0065; metalworking/plasticworking machine operators: OR 1.6, 95% CI 1.01 to 2.6, p(trend) = 0.047). Other occupations/industries for which risk increased significantly with duration of employment included: for men, textile machine operators, mechanics/repairers, automobile mechanics, plumbers, computer systems analysts, information clerks, and landscape industry workers; for women, service occupations, health services, cleaning and building services, management-related occupations, electronic components manufacturing and transportation equipment manufacturing. Men reporting use of metalworking fluids (MWF) had a significantly elevated bladder cancer risk (OR 1.7, 95% CI 1.1 to 2.5).

Our findings support the hypothesis that some component(s) of MWF may be carcinogenic to the bladder. Our results also corroborate many other previously reported associations between bladder cancer risk and various occupations. More detailed analyses using information from the study's job-specific questionnaires may help to identify MWF components that may be carcinogenic, and other bladder carcinogens associated with a variety of occupations.

Lead, a major contaminant, is highly used in paint manufacturing due to its anticorrosive properties. Recent reports indicated high lead content among Indian paints used for commercial purposes. Painters are continuously exposed to these lead containing paints during painting of both commercial as well as residential buildings. Lead is well-known for its genotoxicty in occupational workers; however, in Indian painters the genotoxic effects of lead have not been reported to date. Therefore we aimed to study the genotoxic end points in painters due to their long-term exposure to these high lead-containing Indian paints.

Study group selection was made after a questionnaire administration, which included questions about lifestyle and medical history to exclude exposure to the other potential sources of genotoxics. Blood and buccal cell samples were obtained from 30 male painters and from a similar number of age-matched controls of same location with no occupational exposure to lead. Blood lead levels (Pb-B) were measured in painters and controls. Micronucleus (MN) frequencies and nuclear changes, i.e., karyorrhexis, karyolysis, broken egg, and binucleated, were investigated in buccal epithelial cells.

Painters had significantly (P < 0.01) greater lead levels in blood than the control group. MN frequencies and nuclear changes in buccal epithelial cells were also significantly (P < 0.01) elevated in painters as compared with control subjects. Regression analysis also revealed significant (P < 0.01) association of Pb-B with all the genotoxic endpoints in painters. Cytogenetic damage was significantly associated with Pb-B as no other co-founding factors (smoking, alcohols) showed significant difference between both groups.

Lead is widely used in paints which may serve as potential source of exposure among painters due to their long-term engagement with paints. Our results clearly demonstrated genotoxicity among the exposed population as evident from increase micronucleus frequencies, frequent nuclear changes, and apoptosis. Many studies had previously related nuclear change events in buccal epithelial cells with the progression of different carcinomas. Furthermore in-depth investigations with larger sample size are needed to provide evidence to this effect.

Here, we report cytogenetic toxicity to the exposed population by the high lead containing paints from India for the first time. Frequent, high and unregulated use of lead in paints may cause genetic mutation and may accelerate cytogenetic damage which may further lead to different carcinomas in painters. These findings need to be considered and necessary steps should be taken to protect the occupational workers engaged with these high lead-containing paints.

The use of lead in paints is completely unregulated in India and routine surveillance of paints for lead content is still lacking. These paints are readily available in markets and are also used in other products (jewelry, miniblinds) which could be exported to other countries including United States and Europe. Serious consideration should be given to the inclusion of regulations and bans on the use of lead in paints. Moreover, attention should also be paid towards the use of various protective measures (face-masks, hand gloves, and separate clothes) by the workers as safe work practices during working periods.

In this study, the comet assay was used to evaluate whether welding fume and solvent base paint exposure led to DNA damage in construction-site workers in Turkey. The workers (n = 52) were selected according to their exposure in the construction site and controls (n = 26) from the general population, with no history of occupational exposure. The alkaline comet assay, a standard method for assessing genotoxicity, has been applied in peripheral lymphocytes of all subjects. The mean percentages of DNA in tail (%DNA(T)) of each group were evaluated, including the comparisons between smokers in each different group and the duration of exposure. Significant increase in the mean %DNA(T) (p < 0.01) was observed in all exposed subjects (12.34 ± 2.05) when compared with controls (6.64 ± 1.43). Also %DNA(T) was significantly high (p < 0.01) in welders (13.59 ± 1.89) compared with painters (11.10 ± 1.35). There was a statistical meaningful difference in % DNA(T) between control and exposed smokers. Our findings indicate that exposure to welding fumes and paints induce genotoxic effect in peripheral lymphocytes, indicating a potential health risk for workers. Therefore, to ensure maximum occupational safety, biomonitoring is of great value for assessing the risk for construction workers.

The International Agency for Research on Cancer (IARC) classified occupational painting as a human carcinogen based on lung and bladder cancers; however, no specific exposures were implicated. The authors conducted comprehensive meta-analyses of the epidemiological literature on occupational painting and these cancers. The authors abstracted study results and confounder information, and used quantile plots and regression models to evaluate heterogeneity and publication bias. Summary risk estimates were derived and sensitivity analyses performed to evaluate smoking, socioeconomic status (SES), and exposure variables. Where applicable, a Bayesian approach was used to externally adjust for smoking, a major risk factor for both cancers. For lung cancer cohort mortality studies, publication bias and heterogeneity were seen, and earlier studies reported higher risk estimates than later studies. Overall lung cancer summary risk estimates were 1.29 for case-control and 1.22 and 1.36 for cohort morbidity and mortality studies, respectively, and risk estimates for bladder cancer were 1.28 for case-control and 1.14 and 1.27 for cohort morbidity and mortality studies, respectively (all statistically significant). Risks did not differ between painters and mixed occupations. Nonsignificant summary estimates resulted for lung and bladder cancers when controlling for SES, or externally adjusting for smoking in lung cancer studies. Summary risks varied by control source for case-control studies. Residual confounding by smoking and SES, lack of exposure group effect, and publication bias limit the ability of the meta-analyses to explain associations observed between occupational painting and lung and bladder cancers. Given the long latencies for lung and bladder cancers, these weak associations, if real, may not be elucidated through studies of occupational painting today.

We conducted a meta-analysis to quantitatively compare the association between occupation as a painter and the incidence or mortality from lung cancer.

PubMed and the reference lists of pertinent publications were searched and reviewed. For the meta-analysis, we used data from 47 independent cohort, record linkage, and case control studies (from a total of 74 reports), including > 11,000 incident cases or deaths from lung cancer among painters.

Three authors independently abstracted data and assessed study quality.

The summary relative risk (meta-RR, random effects) for lung cancer in painters was 1.35 [95% confidence interval (CI), 1.291.41; 47 studies] and 1.35 (95% CI, 1.211.51; 27 studies) after controlling for smoking. The relative risk was higher in never-smokers (meta-RR = 2.00; 95% CI, 1.093.67; 3 studies) and persisted when restricted to studies that adjusted for other occupational exposures (meta-RR = 1.57; 95% CI, 1.212.04; 5 studies). The results remained robust when stratified by study design, sex, and study location and are therefore unlikely due to chance or bias. Furthermore, exposure response analyses suggested that the risk increased with duration of employment.

These results support the conclusion that occupational exposures in painters are causally associated with the risk of lung cancer.

We investigated the association between exposure to various groups of solvents and gasoline vapors and liver cancer. A cohort of economically active Finns born between 1906 and 1945 was followed up during the period 1971-1995. The incident cases of primary liver cancer (n = 2474) were identified in a record linkage with the Finnish Cancer Registry. Occupations from the 1970 census were converted to exposures using a job-exposure matrix. Cumulative exposure was calculated as the product of estimated prevalence, level and duration of exposure, and we used Poisson regression to calculate the relative risks (RR). Among the occupations entailing exposure to organic solvents, an elevated liver cancer incidence was observed in male printers, and varnishers and lacquerers. Among men, the risk was increased in the highest exposure category of aromatic hydrocarbons [RR 1.77, 95% confidence interval (CI) 1.30-2.40], aliphatic/alicyclic hydrocarbons (RR 1.47, 95% CI 0.99-2.18), chlorinated hydrocarbons (RR 2.65, 95% CI 1.38-5.11) and "other solvents" (RR 2.14, 95% CI 1.23-3.71). Among women, the risk was increased for the group "other solvents" that includes mainly alcohols, ketones, esters and glycol ethers (RR 2.73, 95% CI 1.21-6.16). Our finding of an increased risk among workers exposed to chlorinated hydrocarbons is in line with several earlier studies on trichloroethylene. The results also suggest a link between exposure to other types of solvents and the risk of liver cancer. The possibility that alcohol consumption contributes to the observed risks cannot be totally excluded.

Painters are considered to be at increased risk of lung cancer. The objective was to evaluate risk of several cancers, apart from lung, in painting-related professions. Most previous studies have focused on the job title rather than on exposures incurred.

A large population based case-control study was carried out during 1979-1986 in Montreal including several types of cancer and focusing on occupational exposures. Interviews elicited detailed lifetime job histories; those were evaluated by a team of industrial hygienists to assign exposure. The exposure checklist included three paint-related substances: metal coatings, wood varnishes and stains, and wood and gypsum paints. Seven types of cancer were analyzed (numbers interviewed): esophagus (97), stomach (248), colorectal (754), prostate (438), bladder (478), kidney (174) and non-Hodgkin's lymphoma (215). For each cancer type, a pooled control group was constituted from 533 population controls and 533 cancer patients selected from other types of cancer. Odds ratios (ORs) were estimated between each of the paint-related agents and each of the seven cancer types, adjusting for several potential confounders, including smoking.

The job title of "painters" was not associated with risk of any of the cancers under study. Most of the ORs between the three agents and the seven cancers were close to null. However, there was a tendency for ORs to be above 1.0 for subjects who had substantial exposure to metal coatings, with noteworthy associations for cancers of the esophagus (OR = 4.2; 95% CI: 1.1-17.0; n = 4), prostate (OR = 2.7; 95% CI: 1.0-7.7; n = 13), and bladder (OR = 1.7; 95% CI: 0.7-4.4; n = 13).

These results are compatible with an absence of risk among painting-related professions; they are also compatible with excess risk of certain cancers, especially among those exposed to metal coatings.

The non-Hodgkin lymphomas (NHL) are a heterogeneous group of B-cell and T-cell neoplasms that arise primarily in the lymph nodes. NHL incidence rates in the US doubled between about 1970 and 1990, and stabilized during the 1990s. NHL accounts for approximately 3.4% of cancer deaths in the US. Although some of the observed patterns in NHL have been related to HIV/AIDS, these conditions cannot fully explain the magnitude of the changes; neither do changes in classification systems nor improved diagnostic capabilities. Studies of occupational and environmental exposures (e.g., pesticides, solvents) have produced no consistent pattern of significant positive associations. Inverse associations with ultraviolet radiation exposure and alcohol and fish intake, and positive associations with meat and saturated fat intake have been reported in several studies; additional studies are needed to confirm or refute these associations. Family history of NHL or other hematolympho-proliferative cancers and personal history of several autoimmune disorders are associated with increased risk of NHL, but are not likely to account for a large proportion of cases. HIV and other infectious agents, such as human herpesvirus 8 and Epstein-Barr, appear to be associated with differing types of NHL, such as some B-cell lymphomas. Future epidemiologic studies should evaluate associations by NHL type, enhance exposure information collected, and elucidate factors that may identify susceptible (or resistant) subpopulations because of genetic, immunologic or other characteristics. The extent to which the etiology of NHL types may differ is important to resolve in ongoing and future studies.

Multiple myeloma, a neoplasm of plasma cells, accounts for approximately approximately 15% of lymphatohematopoietic cancers (LHC) and 2% of all cancers in the US. Incidence rates increase with age, particularly after age 40, and are higher in men, particularly African American men. The etiology is unknown with no established lifestyle, occupational or environmental risk factors. Although several factors have been implicated as potentially etiologic, findings are inconsistent. We reviewed epidemiologic studies that evaluated lifestyle, dietary, occupational and environmental factors; immune function, family history and genetic factors; and the hypothesized precursor, monoclonal gammopathies of undetermined significance (MGUS). Because multiple myeloma is an uncommon disease, etiologic assessments can be difficult because of small numbers of cases in occupational cohort studies, and few subjects reporting exposure to specific agents in case-control studies. Elevated risks have been reported consistently among persons with a positive family history of LHC. A few studies have reported a relationship between obesity and multiple myeloma, and this may be a promising area of research. Factors underlying higher incidence rates of multiple myeloma in African Americans are not understood. The progression from MGUS to multiple myeloma has been reported in several studies; however, there are no established risk factors for MGUS. To improve our understanding of the causes of multiple myeloma, future research efforts should seek the causes of MGUS. More research is also needed on the genetic factors of multiple myeloma, given the strong familial clustering of the disease.

Bladder cancer is a heterogeneous and frequently multifocal disease with a variable clinical course. The management of bladder cancer is therefore challenging and complicated. CT and MR imaging have replaced the traditional excretory urography and are emerging as the imaging modalities of choice for work-up of patients who have bladder cancer. Imaging provides essential diagnostic information for detection, staging, and post-treatment follow-up of bladder cancer.

Case reports and epidemiological studies of workers exposed to benzene have demonstrated associations with a number of lymphohematopoietic diseases, but the association with multiple myeloma (MM) has been less apparent. Data from all of the "benzene cohort studies" conducted to date have been selected and evaluated for inclusion in a meta-analysis. The analysis demonstrates a significant excess in the relative risk (RR) of MM in relation to benzene exposure. Pooling the data from seven cohort studies, a meta-analysis yields a statistically significant weighted RR estimate of 2.13 (95% CI = 1.31-3.46). In the analysis of cohort data, an understanding of the cohort follow-up period in relation to benzene exposure and RR of MM is important. Exposure-related RRs of disease decline after the median latency periods are exceeded, particularly when exposure has terminated decades earlier. The positive epidemiological evidence for benzene as a cause of MM is supported by biological plausibility for such an effect from benzene exposure. Studies of refinery workers are difficult to interpret in relation to benzene exposure and risk of MM, but are limited in the study design and analysis. Nonetheless, they provide some support for an association between refinery work and MM.

Cancer is a health endpoint influenced by a multitude of factors, including genetic history, individual behavior, and environmental insults. The ubiquity of toxicants in the environment has raised questions about the extent of their role in causing cancer in humans. More specifically, it is desirable to understand the cancer incidence due to airborne toxicants in anthropogenic pollution. One particular class of such pollutants is volatile organic compounds (VOCs). This paper reports an epidemiological investigation of the incidence of cancer in the 92 counties of Indiana. We evaluated the relationship between the amount of VOCs released in each county, as reported by the Toxic Release Inventory, and the county-by-county incidence of various types of cancer, especially those of less common organ systems not directly associated with the absorption or distribution of toxicants. Our evaluation considered chlorinated versus nonchlorinated emissions as well as stack versus fugitive emissions. We evaluated three models: linear, quadratic, and polynomial. Of these, the quadratic model appeared to be the best predictor (highest r2) for most endpoints for which there was a positive correlation. However, the linear model was the most sensitive (lowest P-value) for skin, melanoma, and endocrine-related cancers, including female genital system cancers. Our results indicate a relationship between emissions of VOCs and the incidence of some types of cancers. Most notable were strong correlations between VOC emissions and cancers of the brain, nervous system, endocrine system, and skin.

Liver cancer is the fifth most frequent malignancy worldwide. Viral hepatitis B and C, alcohol, and aflatoxin are the major established risk factors. Little is known about the aetiological contributions of occupational exposures, as previous occupational epidemiological studies of liver cancer suggest few agent-specific associations. We investigated associations of occupational exposures to dusts and chemicals in a cohort of female textile workers.

Cancer incidence was determined among 267,400 female textile workers in Shanghai, China, who had been enrolled in an intervention trial of breast self-exam efficacy during 1989-98. Subjects were interviewed at baseline regarding basic demographics, smoking habits, alcohol consumption, and contraceptive practices. A case-cohort study of 360 liver cancer cases and 3,186 age-stratified randomly chosen subcohort subjects was conducted within this cohort. Exposures to workplace dusts and chemicals were reconstructed from complete work history data, historical exposure monitoring data for selected agents, and a specially designed job-exposure matrix for the textile industry. Relative risks and dose-response trends were estimated by Cox proportional hazards modelling, adapted for the case-cohort design. Latency analyses with different lag years were also applied.

2,095,904 person-years were contributed by this female cohort. The results of the case-cohort analysis revealed a protective effect of cotton fibre exposure years [adjusted hazards ratio (HR) = 0.64; 95% confidence interval (95% CI) 0.44-0.92] or endotoxin exposure (adjusted HR = 0.60; 95% CI 0.41-0.88) for the fourth quartile with significant trends for 20 year exposure lags.

This study suggests that chronic exposure to endotoxin or some other component of cotton dust exposure may have reduced liver cancer risk in this population.

Bladder cancer is a heterogeneous disease with a variable natural history. At one end of the spectrum, low-grade Ta tumors have a low progression rate and require initial endoscopic treatment and surveillance but rarely present a threat to the patient. At the other extreme, high-grade tumors have a high malignant potential associated with significant progression and cancer death rates. In the Western world, bladder cancer is the fourth most common malignancy in men and the eighth most common in women. In Europe and the United States, bladder cancer accounts for 5% to 10% of all malignancies in men. The risk of developing bladder cancer at <75 years of age is 2% to 4% for men and 0.5% to 1% in women compared with the risk of lung cancer, for example, which is 8% in men and 2% in women. For the geographic and temporal comparison of bladder cancer incidence, it is crucial to separate the low-grade from the high-grade tumors. In epidemiologic studies on risk factors for bladder cancer, it is important to distinguish the low-grade Ta tumors from high-grade carcinoma in situ (CIS) and tumors >T1. Current studies do not support the routine screening for bladder cancer. However, prospective long-term studies are required to evaluate the benefits of bladder cancer screening, particularly in those at high risk. After assessing all available evidence, the Epidemiology and Diagnosis Committee has made recommendations on various diagnostic issues, including pathologic evaluation, urinary cytology, and imaging studies. Optimal resection techniques, role of repeat transurethral resection in high-grade T1 tumors, random bladder biopsy, and prostatic urethral biopsy are discussed, and appropriate recommendations are made according to the strength of available evidence.

Epidemiological studies on the potential association between painting and the risk of bladder cancer published after the Monograph of the International Agency for Research on Cancer N. 47 of 1989 have been systematically reviewed. These included four cohort studies on the incidence of bladder cancer among painters, with a pooled relative risk (RR) of 1.10 (95% confidence interval, CI, 1.03-1.18), based on 893 cases observed. The corresponding summary RR from four cohort studies on mortality was 1.23 (95% CI 1.11-1.37), based on 370 deaths. The pooled RR from 14 case-control studies and a pooled-analysis of other 11 case-control studies was 1.35 (95% CI 1.19-1.53), based on 465 cases exposed. Overall, the RR from all epidemiological studies was 1.17 (95% 1.11-1.27). Thus, recent epidemiological evidence indicates a moderate excess risk for bladder cancer in painters. Some studies, however, suggested that any such risk would have been greater for exposures in the distant past. Open issues for interpretation include residual confounding by social class and tobacco smoking, and understanding the time-risk relation. In particular, the potential residual risk related to exposure over the last two to three decades remains to be defined.

To identify which cases of adult bladder cancer notified to the New Zealand Cancer Registry in 2001 had a probable occupational cause.

Occupational Safety and Health (OSH), in conjunction with the Massey University Centre for Public Health Research, interviewed and obtained an occupational history for 210 (162 men, 48 women) cases.

Of the 162 male cases (response rate 65%), 45 (28%) were considered to be 'probable' occupational cancers. Of the 48 female cases (response rate 76%), three cases (6%) were considered to be 'probable' occupational cancers. The largest occupational group for men was truck drivers, which made up 51% of probable cases. Other common groups were engineering and metal workers (18%), crop farmers/orchardists (7%), textile and leather workers (7%), painters/furniture finishers (7%), and plastics manufacturing workers (4%). The three female cases considered to be of occupational origin included two textile workers and one telephonist.

The percentage of cases considered to be of occupational origin is similar to that reported in Europe and the United States, indicating that occupational cancer is a major occupational health problem in New Zealand as it is in other parts of the world.

To investigate occupational risk factors for bladder cancer in seven Canadian provinces.

We analysed a population-based case-control dataset of 887 individuals with incident, histologically confirmed bladder cancer between 1994 and 1997. Controls (2847) frequency matched for age and gender were surveyed in 1996. Questionnaires were returned by about 60% of subjects. Odds ratios (ORs) for occupations and self-reported exposures were adjusted for province, age, race, smoking, and several dietary factors, using unconditional logistic regression.

Statistically significant increased risks were observed among men employed as hairdressers (OR = 3.42; 1.09-10.8), primary metal workers (OR = 2.40; 1.29-4.50), miners (OR = 1.94; 1.18-3.17), and automechanics (OR = 1.69; 1.02-2.82). Primary metal workers and automechanics showed evidence of an employment duration-response trend. Modest elevated risks that were not significant were also observed for male government inspectors, printers, firefighters, general labourers, and welders. A duration-response trend was evident for government inspectors and general labourers. For females, significant elevations were observed among lumber processors (OR = 8.78; 1.28-60.1), general labourers (OR = 2.18; 1.05-4.52), nurses (OR = 1.54; 1.03-2.31), and general clerks (OR = 1.48; 1.01-2.17). The latter showed a positive duration-response trend.

This study found a statistically significant excess risk of bladder cancer, with a duration-response trend, among male primary metal workers and automechanics, and female office workers engaged in general clerical duties.

Occupational exposure is definitely a major cause of cancer. In the field of urology, the urinary bladder is the most important target. A classical cause of bladder cancer is exposure to carcinogenic aromatic amines, especially benzidine and beta-naphthylamine. Such exposures were related to work places in the chemical industry, implying production and processing of classical aromatic amines, and in the rubber industry. Occupational bladder cancer has also been observed in dyers, painters and hairdressers. Even some occupations with much lower exposures to carcinogenic aromatic amines, like coke oven workers or workers in the rubber industry after the ban on beta-naphthylamine, are at risk. In these occupations, exposure to complex mixtures of substances containing combustion products (e.g. polycyclic aromatic hydrocarbons) or nitrosamines is common. Renal cell cancer has been observed as an occupational disease in cases of very high exposure to trichloroethylene having led to narcotic or prenarcotic symptoms. Occupationally related cancers of the prostate or the testes appear currently not relevant.

Shipbuilding workers are exposed to a variety of genotoxic compounds including polycyclic aromatic hydrocarbons (PAHs). A limited number of studies have been conducted to evaluate biomarkers related to PAH exposure in painters in the shipyard industry. We examined this in 208 workers recruited from a shipyard located in South Korea. Employees were grouped into three exposure groups: (1) 111 painters using coal tar paints, (2) 70 painters using general paints, and (3) 27 on-site controls using no paints. Levels of urinary 1-hydroxypyrene glucuronide (1-OHPG), as internal dose of PAH exposure, were measured by synchronous fluorescence spectroscopy. Glutathione S-transferase (GST) M1 and T1 genotypes were assessed by a multiplex polymerase chain reaction (PCR)-based method, aromatic-DNA adducts in peripheral white blood cells were measured by 32P-postlabeling, and glycophorin A (GPA) variant frequencies in red blood cells were assessed by flow cytometry. Information on demographic characteristics, smoking habits, diet, job title and use of personal protective equipment (e.g. respiratory and dermal) were collected by self-administered questionnaire. Average urinary 1-OHPG levels in coal tar paint (2.24 micromol/mol creatinine) and general paint (1.38 micromol/mol creatinine) users were significantly higher than in on-site controls (0.62 micromol/mol creatinine) (P<0.001). Paint use, irrespective of the type of paints, and smoking (yes/no) were positively associated with urinary 1-OHPG levels, whereas green tea consumption (yes/no) was negatively associated with the 1-OHPG levels. No significant effect in the 1-OHPG levels were observed for the GSTM1 and GSTT1 genotypes. Aromatic-DNA adduct levels tended to be higher in coal tar paint users (P = 0.06) and painters (P = 0.07) compared to on-site controls. No differences in adduct levels were observed, between the two groups of painters, and the combined group showed greater adduct levels than on-site controls (P = 0.05). GPA mutation frequencies measured in 55 individuals with MN heterozygote genotypes were not significantly different among the three exposure groups, and no correlation was observed between urinary 1-OHPG levels and aromatic-DNA adducts or GPA mutation frequency. These results suggest that painters in the shipyard were exposed to significant amounts of PAHs and possibly to other genotoxic aromatic compounds, and that urinary 1-OHPG may be a potential biomarker of PAH exposure in this population.

Asbestosis can cause significant impairment and even death. It is also a well-recognized risk factor for the development of lung cancer. However, asbestosis is usually diagnosed on clinical grounds without the aid of pathology. Many physicians and researchers believe that in asbestos-exposed individuals with adequate latency, chest radiographic findings that are compatible with asbestosis are sufficient for the diagnosis. In order to determine whether this approach is reasonable, the positive predictive value of the chest radiograph for the diagnosis of pathologic asbestosis must be determined. This requires information about the prevalence of asbestosis, and the sensitivity and specificity of the chest radiograph in its diagnosis. In this article, the sensitivity and specificity of the chest radiograph in diagnosing asbestosis is determined from a literature analysis. The prevalence of asbestosis among present-day cohorts, such as construction workers and petrochemical workers, is assessed based on the relative risk of lung cancer in patients with asbestosis and the overall relative risk of lung cancer in these occupationally asbestos-exposed cohorts. The results indicate a positive predictive value for abnormal chest radiograph findings alone to be significantly < 50%. Therefore, the chest radiograph is inadequate as the sole clinical tool to be used to diagnose asbestosis in these cohorts. However, when rales and a low diffusing capacity of the lung for carbon monoxide are also present, the diagnosis of asbestosis on clinical grounds can be made with reasonable confidence.

Bladder cancer is currently diagnosed using cystoscopy and cytology in patients with suspicious signs and symptoms. These same tests are used to monitor patients with a history of bladder cancer for recurrence. The recurrence rate for bladder cancer is high, thus necessitating long-term follow-up. Urine cytology requires an experienced cytopathologist and is costly. It has high specificity, but low sensitivity for low-grade bladder tumors. Recently many non-invasive bladder cancer tests, utilizing markers found in the urine, have been developed. The FDA has approved several of these for the use is bladder cancer diagnosis, and many others are undergoing development and investigation. An ideal bladder cancer test would be non-invasive, highly sensitive and specific, inexpensive, easy to perform, and yield highly reproducible results. Many of the tests reviewed meet some, but not all, of these criteria.

Lung cancer is associated with occupation, but not much is known about the influence exerted on risk by length of exposure and the joint effect of occupational exposure and tobacco on risk of lung cancer.

Through a population-based case-control study, we defined risk professions as those that have been associated previously with higher risk of lung cancer.

The relative risk seems to increase linearly and significantly with the number of years spent in risk occupations, rising significantly by 28% for every 10 years in a risk profession. Should such occupations be combined with exposure to a smoking habit, then in the case of heavy smokers, a working career spanning 20 years or more in risk occupations would mean tripling the possibility of developing lung cancer from occupation.

The high risks observed indicate a public health problem and indicate that joint exposure to risk professions and tobacco ought to be avoided. We must stress from these results the need for effective education for all workers.

While considerable efforts have been made to investigate the role of occupation and industry in the risk of bladder cancer, many reported associations have not been consistent, and strong evidence of increased risk is apparent for few occupational groups. To further examine the issue, a large, population-based, case-control study was conducted in the state of Iowa among both men and women. A total of 1452 incident bladder cancer cases and 2434 controls were included in the study. Occupational history was collected from respondents for each job held for 5 years or longer since age 16. Among men, excess risk was observed for industries including plumbing, heating, and air conditioning (odds ratio [OR], = 2.2; 95% confidence interval [CI], 1.0 to 5.0); rubber and plastic products (OR = 3.1; 95% CI, 1.2 to 8.5), motor vehicle parts and supplies (OR = 4.5; 95% CI, 1.2 to 16.5), and occupations including supervisors for transportation and material moving (OR = 6.5; 95% CI, 1.4 to 29.9), material-moving-equipment operators (OR = 1.9; 95% CI, 1.0 to 3.6), automobile mechanics (OR = 1.6; 95% CI, 1.0 to 2.6), painters (OR = 2.7; 95% CI, 1.0 to 7.7), and metal- and plastic-working machine operators (OR = 2.0; 95% CI, 1.1 to 3.4). Among women, significant excess risk was observed for secondary school teachers and record clerks. Housekeepers and butlers and workers in laundering and dry cleaning were also at increased risk. In conclusion, these results suggest that occupational exposures may play a significant role in the risk of bladder cancer.

Human bladder cancer may be caused by exposure to aromatic amines. The polymorphic enzyme N-acetyltransferase 2 (NAT2) is involved in the metabolism of these compounds. Two classical studies on chemical workers in Europe, exposed in the past to aromatic amines like benzidine, unambiguously showed that the slow acetylator status is a genetic risk factor for arylamine-induced bladder cancer. In the former benzidine industry in Huddington, Great Britain, 22 of 23 exposed cases with bladder cancer, but only 57% of 95 local controls without bladder cancer were of the slow acetylator phenotype. In Leverkusen, Germany, 82% of 92 benzidine-exposed chemical workers with bladder cancer were of the slow acetylator phenotype, whereas only 48% of 331 chemical workers who had worked at that plant were of the slow acetylator phenotype. This is in line with several smaller studies, which also show an over-representation of the slow acetylator status in formerly arylamine-exposed subjects with bladder cancer. Some of these studies included also subjects that were exposed to aromatic amines by having applied dyes, paints and varnishes. These European findings are in contrast to a large study on Chinese workers occupationally exposed to aromatic amines. In this study, only five of 38 bladder cancer cases occupationally exposed to arylamines were of the slow acetylator genotype. This is much lower than the ratio of slow acetylators to the general population in China. This points to different mechanisms of susceptibility for bladder cancer upon exposure to aromatic amines between European (Caucasian) and Chinese populations.

Using data from the 1960 and 1970 Swedish censuses and the Swedish Cancer Register for 1971 to 1989, this study investigated variations in cancer risk by gender associated with employment in painting trades and paint manufacturing. Among men, standardized incidence ratios were significantly increased for lung cancer among painters and lacquerers; bladder cancer among artists; and pancreas cancer, lung cancer, and nonlymphocytic leukemia among paint and varnish plant workers. Risks for women were elevated for cancers of the esophagus, larynx, and oral cavity among lacquerers and for oral cancer among glaziers. These findings are consistent with the report of the International Agency for Research on Cancer that classified painting as an occupationally related cause of cancer and provide further evidence that the risk of certain cancers is increased by exposures in the paint manufacturing process.

The transfer efficiency of a compressed air spray gun is an important performance index with regard to worker health, environmental, and economic considerations. It is defined as the fraction of paint sprayed that coats the surface. Worker exposure has been identified as a function of the transfer efficiency based on total mass of paint sprayed, which can be predicted by a mathematical model developed with nonvolatile oil. This study extends the existing model to include volatile effects by employing a mathematical approach based on a mass balance. This method allows the current model to predict transfer efficiency bounds at two extreme situations: all volatile compounds evaporate either before or after droplet impaction. Model predictions show that tight transfer efficiency bounds are obtained, especially for high values of transfer efficiency. Thus, the average of the upper and lower bounds should be a reasonable estimate of transfer efficiency. It is also found that the current model prediction, which is based on total mass of paint sprayed, for nonvolatile material can be converted to a transfer efficiency based on the mass of solids. The laboratory study shows that the predicted transfer efficiency based on the mass of solids is within the 95 percent C.I. of the measured value. This work relates the transfer efficiency used in industry, which is calculated on the basis of paint solids, with a model that predicts worker exposure during spray painting operations.