Benzene exposure has been shown to be related to acute myelogenous leukemia, while the association with multiple myeloma and non-Hodgkin lymphoma has been a much-debated issue. We performed a historical cohort study to investigate whether workers employed in Norway's upstream petroleum industry exposed to crude oil and other products containing benzene have an increased risk of developing various subtypes of hematologic neoplasms. Using the Norwegian Registry of Employers and Employees we included all 27,919 offshore workers registered from 1981 to 2003 and 366,114 referents from the general working population matched by gender, age, and community of residence. The cohort was linked to the Cancer Registry of Norway. Workers in the job category "upstream operator offshore", having the most extensive contact with crude oil, had an excess risk of hematologic neoplasms (blood and bone marrow) (rate ratio (RR) 1.90, 95% confidence interval (95% CI): 1.19-3.02). This was ascribed to an increased risk of acute myelogenous leukemia (RR 2.89, 95% CI: 1.25-6.67) and multiple myeloma (RR 2.49, 95% CI: 1.21-5.13). There were no statistical differences between the groups in respect to non-Hodgkin lymphoma. The results suggest that benzene exposure, which most probably caused the increased risk of acute myelogenous leukemia, also resulted in an increased risk of multiple myeloma.

Use of the general population as a reference might cause serious underestimation of the risk of cancer in working populations because of the healthy worker effect. Using incidence rates, we studied how this underestimation varied according to subtypes of cancer by comparing a large cohort of randomly selected Norwegian workers hired between 1981 and 2003 (n = 366,114) with the general Norwegian population. The cohort was linked to the Cancer Registry of Norway, including all new cancer cases (n = 11,271) reported up to 2003. We found marked potential for the healthy worker effect for overall cancer incidence in male workers (standardized incidence ratio (SIR) = 0.91, 95% confidence interval: 0.89, 0.93) but not in female workers (SIR = 0.99, 95% confidence interval: 0.95, 1.03). A statistically significantly lower incidence was found among men for cancers of the head and neck (SIR = 0.78), lung (SIR = 0.81), prostate (SIR = 0.93), kidney (SIR = 0.83), and bladder (SIR = 0.77) and for leukemia (SIR = 0.80), whereas an increased incidence was found for malignant melanoma among both men (SIR = 1.09) and women (SIR = 1.29) and for ovarian cancer in women (SIR = 1.32). Depending on the type of cancer being studied, marked potential exists for both underestimation and overestimation of cancer risk when the general population is used as the reference for studies of worker populations.

Background: Overweight status and asthma have increased during the last decades. Being overweight is a known risk factor for asthma, but it is not known whether it might also increase asthma risk in the next generation. Objective: We aimed to examine whether parents being overweight in childhood, adolescence, or adulthood is associated with asthma in their offspring. Methods: We included 6347 adult offspring (age, 18-52 years) investigated in the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) multigeneration study of 2044 fathers and 2549 mothers (age, 37-66 years) investigated in the European Community Respiratory Health Survey (ECRHS) study. Associations of parental overweight status at age 8 years, puberty, and age 30 years with offspring's childhood overweight status (potential mediator) and offspring's asthma with or without nasal allergies (outcomes) was analyzed by using 2-level logistic regression and 2-level multinomial logistic regression, respectively. Counterfactual-based mediation analysis was performed to establish whether observed associations were direct or indirect effects mediated through the offspring's own overweight status. Results: We found statistically significant associations between both fathers' and mothers' childhood overweight status and offspring's childhood overweight status (odds ratio, 2.23 [95% CI, 1.45-3.42] and 2.45 [95% CI, 1.86-3.22], respectively). We also found a statistically significant effect of fathers' onset of being overweight in puberty on offspring's asthma without nasal allergies (relative risk ratio, 2.31 [95% CI, 1.23-4.33]). This effect was direct and not mediated through the offspring's own overweight status. No effect on offspring's asthma with nasal allergies was found.

These findings do not support a major aetiological role of petroleum-based products, but rather point to smoking and other lifestyle factors related to the level of education as being important for the risk of MS.

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