American Cancer Society; Centers for Disease Control and Prevention; Swiss Re; Swiss Cancer Research foundation; Swiss Cancer League; Institut National du Cancer; La Ligue Contre le Cancer; Rossy Family Foundation; US National Cancer Institute; and the Susan G Komen Foundation.

Purpose In contrast to other US racial/ethnic groups, Asian Americans (AA) have experienced steadily increasing breast cancer rates in recent decades. To better understand potential contributors to this increase, we examined incidence trends by age and stage among women from seven AA ethnic groups in California from 1988 through 2013, and incidence patterns by subtype and age at diagnosis for the years 2009 through 2013. Methods Joinpoint regression was applied to California Cancer Registry data to calculate annual percentage change (APC) for incidence trends. Incidence rate ratios were used to compare rates for AA ethnic groups relative to non-Hispanic whites (NHW). Results All AA groups except Japanese experienced incidence increases, with the largest among Koreans in 1988–2006 (APC: 4.7, 95% CI: 3.8, 5.7) and Southeast Asians in 1988–2013 (APC: 2.5, 95% CI: 0.8, 4.2). Among women younger than age 50, large increases occurred for Vietnamese and other Southeast Asians; among women over age 50, increasing trends occurred in all AA ethnic groups. Rates increased for distant stage disease among Filipinas (2.2% per year, 95% CI: 0.4, 3.9). Compared to NHW, Filipinas and older Vietnamese had higher incidence rates of some HER2+ subtypes. Conclusions Breast cancer incidence rates have risen rapidly among California AA, with the greatest increases in Koreans and Southeast Asians. Culturally-tailored efforts to increase awareness of and attention to breast cancer risk factors are needed. Given the relatively higher rates of HER2-overexpressing subtypes in some AA ethnicities, research including these groups and their potentially unique exposures may help elucidate disease etiology.

The incidence of colorectal cancer in the United States declined substantially over the past 20 years, but evidence suggests that among younger adults (under 50 years at diagnosis), incidence is increasing. However, data on age- and stage-specific incidence trends across racial/ethnic groups are limited. All incident cases of colorectal cancer diagnosed from 1990 through 2014 in adults aged 20 years and older were obtained from the California Cancer Registry. Incidence rates (per 100,000), incidence rate ratios, and triannual percent changes in incidence were estimated for each age group at diagnosis (20-49, 50-74, 75+ years), sex, stage, and race/ethnicity (non-Hispanic white, non-Hispanic black, Hispanic, and 7 Asian American groups). Of 349,176 incident colorectal cancer cases diagnosed from 1990 through 2014, 9% were in adults younger than 50 years. Increases in incidence of early-onset colorectal cancer, especially in regional/distant stage disease, were observed in most racial/ethnic groups (statistically significant for non-Hispanic whites and Hispanics, ranging from 0.9% to 2.9% every 3 years). Incidence also increased in Vietnamese and other Southeast Asian groups of screening age (50-74 years). The incidence of colorectal cancer in non-Hispanic blacks aged 50+ declined over the 25-year period, but remained significantly higher than in non-Hispanic whites. Further research is needed to understand the causes of the increasing incidence of early-onset colorectal cancer. The rising incidence of colorectal cancer among Southeast Asians of screening age and the persistently high incidence in non-Hispanic blacks also warrant attention. Our findings may have implications for revisiting screening guidelines in the United States. .

Numerous investigators have suggested that there is likely to be a cumulative chrysotile exposure below which there is negligible risk of asbestos-related diseases. However, to date, little research has been conducted to identify an actual "no-effect" exposure level for chrysotile-related lung cancer and mesothelioma. The purpose of this analysis is to summarize and present all of the cumulative exposure-response data reported for predominantly chrysotile-exposed cohorts in the published literature. Criteria for consideration in this analysis included stratification of relative risk or mortality ratio estimates by cumulative chrysotile exposure. Over 350 studies were initially evaluated and subsequently excluded from the analysis due primarily to lack of cumulative exposure information, lack of information on fiber type, and/or evidence of significant exposures to amphiboles. Fourteen studies meeting the inclusion criteria were found where lung cancer risk was stratified by cumulative chrysotile exposure; four such studies were found for mesothelioma. All of the studies involved cohorts exposed to high levels of chrysotile in mining or manufacturing settings. The preponderance of the cumulative "no-effects" exposure levels for lung cancer and mesothelioma fall in a range of approximately 25-1,000 fibers per cubic centimeter per year (f/cc-yr) and 15-500 f/cc-yr, respectively, and a majority of the studies did not report an increased risk at the highest estimated exposure. Sources of uncertainty in these values include errors in the cumulative exposure estimates, conversion of dust counts to fiber data, and use of national age-adjusted mortality rates. Numerous potential biases also exist. For example, smoking was rarely controlled for and amphibole exposure did in fact occur in a majority of the studies, which would bias many of the reported "no-effect" exposure levels towards lower values. However, many of the studies likely lack sufficient power (e.g., due to small cohort size) to assess whether there could have been a significant increase in risk at the reported no-observed-adverse-effects level (NOAEL); additional statistical analyses are required to address this source of bias and the attendant influence on these values. The chrysotile NOAELs appear to be consistent with exposure-response information for certain cohorts with well-established industrial hygiene and epidemiology data. Specifically, the range of chrysotile NOAELs were found to be consistently higher than upper-bound cumulative chrysotile exposure estimates that have been published for pre-1980s automobile mechanics (e.g., 95th percentile of 2.0 f/ cc-yr), an occupation that historically worked with chrysotile-containing friction products yet has been shown to have no increased risk of asbestos-related diseases. While the debate regarding chrysotile as a risk factor for mesothelioma will likely continue for some time, future research into nonlinear, threshold cancer risk models for chrysotile-related respiratory diseases appears to be warranted.

The potential for para-occupational (or "take-home") exposure to a number of chemicals has been recognized for over 60 years. We conducted a literature review in order to characterize reported cases of asbestos-related disease among household contacts of workers occupationally exposed to asbestos. Over 200 published articles were evaluated. Nearly 60 articles described cases of asbestos-related disease thought to be caused by para-occupational exposure. Over 65% of these cases were in persons who lived with workers classified as miners, shipyard workers, insulators, or others involved in the manufacturing of asbestos-containing products, with nearly all remaining workers identified as craftsmen. 98% of the available lung samples of the persons with diseases indicated the presence of amphibole asbestos. Eight studies provided airborne asbestos concentrations during (i) handling of clothing contaminated with asbestos during insulation work or simulated use of friction products; (ii) ambient conditions in the homes of asbestos miners; and (iii) wearing previously contaminated clothing. This review indicates that the literature is dominated by case reports, the majority of which involved household contacts of workers in industries characterized, generally, by high exposures to amphiboles or mixed mineral types. The available data do not implicate chrysotile as a significant cause of disease for household contacts. Also, our analysis indicates that there is insufficient information in the published literature that would allow one to relate airborne asbestos concentrations in a workplace to those that would be generated from subsequent handling of contact with clothing that had been contaminated in that environment. Ideally, a simulation study could be conducted in the future to better understand the relationships between the airborne concentrations in the workplace and the fiber characteristics that influence retention on fabric, as well as the concentrations that can be generated by handling the contaminated clothing by the persons in the home.