This population-based case–referent study aimed to identify occupational exposures related to elevated risk of lung cancer among lifelong nonsmoking Chinese men in Hong Kong. We found that the groups with employment as ‘bricklayers, carpenters, and other construction workers' or occupational exposure to silica dust, diesel exhaust, or painting were associated with a significantly increased risk of lung cancer. On account of the small number of subjects in each specific industry or occupation, we analysed risk in major industrial and occupational groups, and found an increased risk of lung cancer among men who had ever been employed as ‘bricklayers, carpenters, and other construction workers'. In Hong Kong, workers employed in construction and the related work accounts for around 9% of the local workforce, while employment as ‘bricklayers, carpenters, and other construction workers' is the major occupation of local construction industry involving several job tasks, such as stone cutting, pneumatic drilling, caisson, tunnelling, dynamiting, rock sand blasting (already banned), stone crushing, cement machine attendant, bricklayer, decoration work, truck driving or operators of excavating machines, and unskilled labourers (Yu et al, 2007
). These job tasks are frequently linked to several occupational hazards, in particular, silica dust, diesel exhausts, and painting work. All these occupational exposures are confirmed or suspected as associated with an increased risk of lung cancer (IARC, 1989
Crystalline silica dust has been reclassified as a human group 1 carcinogen by the International Agency for Research on Cancer (IARC) in 1997 (IARC, 1997
), while its carcinogenicity has long been debated as potentially confounding the effect of smoking (McDonald and Cherry, 1999
; Checkoway and Franzblau, 2000
; Hessel et al, 2000
; Pelucchi et al, 2006
). We estimated the independent effect of silica dust in nonsmokers, thus avoiding this problem. A recently published multicentre case–referent study in Europe found an OR of 1.76 (95% CI: 0.97, 3.21) in nonsmoking subjects who had ever been exposed to silica dust, and a higher OR in the longest duration of employment group (OR=2.39, 95% CI: 1.11, 5.15, based on 223 cases of which 48 were male) after adjustment of age, sex, and study centre (Zeka et al, 2006
). The same group of workers found an OR of 1.41 (95% CI: 0.79, 2.49) after redefining the nonexposure group as subjects not exposed to silica dust for >20 years before interview (Cassidy et al, 2007
). We observed an OR of 2.58 among male workers ever exposed to silica dust and a positive association with increasing years of employment. We carried out a sensitivity analysis and found that the risk estimate was almost unchanged (OR=2.55, 95% CI: 1.14, 5.73) after redefining the nonsmoking status as that of the European study – a man who smoked <100 cigarettes in his lifetime (Zeka et al, 2006
). We further re-estimated the results by removing ‘any cancer in first-degree relatives', ‘past history of lung diseases', and ‘meat intake' (these variables were not considered in Cassidy's study) from the model, and found that the OR was reduced by 6.2% (OR=2.42, 95% CI: 1.07, 5.49), but it was still higher than those reported by Zeka et al (2006)
. Our study provides supportive evidence for an independent effect of crystalline silica on lung cancer risk among nonsmokers.
About 18% of our nonsmoking lung cancer cases had been involved in painting work and majority of them were assigned in renovation work of construction or car renewals in which spray painting is frequently required. Employment as a painter has been listed as a human group 1 carcinogen (IARC, 1989
); two recent reviews support the conclusion of IARC after assessing reports on painters published since 1951 and a weak association for lung cancer risk (1.22 and 1.36) was shown after controlling for smoking (Bachand et al, 2010
; Guha et al, 2010
). Occupational exposure as a spray painter has been associated with an increased risk of urinary tract and testicular cancer, whereas its separate effect on lung cancer has not yet been reported (IARC, 1989
). We found a slightly higher risk of lung cancer among painting workers using spray at work (OR=2.81) than general painters whose work never involved spraying (OR=2.36), suggesting exposure differences. Painting workers are commonly exposed by inhalation of solvents and paint dusts (e.g. silica dusts, asbestos dusts, and heavy metals) (IARC, 1989
), while spray painting workers may be additionally exposed to a variety of suspected carcinogens in the form of aerosol or fine particles, which can be readily absorbed deep into the lungs (Sabty-daily et al, 2005
). Our positive association with years of employment as spray painters corroborates the IARC conclusion.
Previous studies showed an average of 33% (95% CI: 24, 44%) excess risk of lung cancer among railroad workers and truck drivers occupationally exposed to diesel engine exhaust emissions, but were commonly criticised for the lack of reliable exposure assessment and inadequate control for smoking. The IARC evaluated diesel exhaust as a group 2A carcinogen because of the limited evidence of carcinogenicity in humans (IARC, 2009
). We observed an OR of 3.47 among nonsmoking men occupationally exposed to diesel exhaust, which is much higher than previously reported, but may well be as only six cases of lung cancer were exposed to diesel exhaust and there was no gradient with duration of employment.
There have been few studies of occupation and histological types of lung cancer among lifelong nonsmoking men. Our study numbers allowed us to explore only the risk of adenocarcinoma (the commonest histological type), and among nonsmoking men, we found a slightly higher association with silica dust exposure (a significant OR retained), but a relatively lower OR for occupational exposure to painting and diesel exhaust than all lung cancer cases. The relatively wide CIs of many of risk estimates indicate our limited powers for investigating associations with adenocarcinoma risk, while the multiple comparisons point to the possibility that some significant results have occurred by chance.
Accuracies in recall of nonsmoking status of our subjects (>0.95) and selection bias for the cases and community referents have been addressed in another paper about ETS and lung cancer (Tse et al, 2009b
). Misclassification of self-reported occupational exposures is a concern because the workers might not accurately identify the specific hazards in their working environments, but these are likely to be nondifferential between cases and referents, resulting in under-estimation of risk. Also, it is difficult to detangle the effects of different job tasks when workers were employed in several occupations during their lifetimes and thus potentially exposed to multiple chemical substances, which indeed may occur even if only one occupation was involved. We are aware that using ‘ever exposure' might not be a good measurement to quantify the independent effect of an occupational exposure. This study is, therefore, only preliminary and needs confirmation.
To further evaluate the potential recall and/or interviewer bias, we interviewed a subgroup of 45 proxy respondents (e.g. spouse) 2 months after the initial interview and found the overall agreement on occupational exposures was excellent (κ=0.72). The test–retest reliability for the same respondents was also very good for both cases (κ=0.65) and referents (κ=0.60). We further interviewed a special group of 64 inpatient referents (who had to undergo surgical operations for suspected lung cancer and were treated as lung cancer cases at the interviews, but eventually were diagnosed as not suffering from lung cancer) who showed a lower proportion of occupational exposures than the confirmed lung cancer cases, suggesting that any interviewer or recall bias was not a major issue.
Our study found that men employed as ‘bricklayers, carpenters, and other construction workers' and those who had ever been occupationally exposed to silica dust, diesel exhaust, and painting work were associated with an increased risk of all lung cancers, and the effects were independent of smoking.