Racial Disparities in Pain Among Women with Fibromyalgia: Secondary Data Analysis of Severity, Interference with Function, and Response to Guided Imagery.

Background: Fibromyalgia syndrome (FMS) is characterized by widespread persistent musculoskeletal pain. Mostly prevalent among White women, little is known about FMS in other population cohorts. This study examined secondary data of a racially diverse sample of women with FMS that were collected as part of a randomized controlled clinical trial that examined the effect of a complementary therapy intervention over the course of a 10-week guided imagery intervention to identify demographic, social, or economic differences in self-reported pain. Materials and Methods: The Brief Pain Inventory (BPI), which measures pain severity and interference, was administered to 72 women (21 Black and 51 Whites) at baseline, 6 and 10 weeks. Student's t tests and time series regression models examined racial difference in pain dimensions and treatment response. Regression models accounted for age, race, income, duration of symptoms, treatment group, pain at baseline, smoking, alcohol use, comorbid conditions, and time. Results: Black women experienced significantly higher pain severity (ß = 5.52, standard deviation [SD] = 2.13) and interference (ß = 5.54, SD = 2.74) than Whites (severity ß = 4.56, SD = 2.08; interference ß = 4.72, SD = 2.76) (interference: t = 1.92, p = 0.05; severity: t = 2.95, p = 0.00). Disparities persisted over time. Controlling for differences in age, income, and previous pain levels, Black women had 0.26 (standard error [SE] = 0.065) higher pain severity and 0.36 (SE = 0.078) higher interference than Whites. Low-income earners also experienced 2.02 (SE = 0.38) and 2.19 (SE = 0.46) higher pain severity and interference, respectively, than other earners. Results were robust to inclusion of comorbidities. Conclusions: Black women and low-income earners experienced significantly higher levels of pain severity and interference and a lower dose response to the intervention. Differentials were robust to inclusion of demographic, health, and behavioral characteristics. Findings suggest that external factors may contribute to pain perception among women with FMS.

Reducing the use of carcinogens: the Massachusetts experience.

Toxics use reduction (TUR) is one part of a comprehensive cancer prevention strategy. TUR emphasizes reducing the use of cancer-causing chemicals by improving manufacturing processes and identifying and adopting safer alternatives. This analysis draws on 20 years of data collected from industries reporting to the Massachusetts Toxics Use Reduction Act (TURA) program to assess trends in the use and release of chemicals associated with cancer. We used a master list of known and suspected carcinogens developed from authoritative sources and a list of carcinogens grouped by their association with 11 cancer sites to analyze trends in use and release of chemicals by industrial facilities reporting to the TURA program from 1990 to 2010. The trend analysis shows that reported use and releases of carcinogens by these Massachusetts companies have decreased dramatically over time. Reported use declined 32% from 1990 to 2010, and reported releases declined 93% from 1991 to 2010 (1991 is when additional industrial sectors, including electric utilities, were phased into the program). Particularly large reductions were achieved in the use of trichloroethylene, perchloroethylene and cadmium and cadmium compounds. The analysis of groups of chemicals associated with specific cancer sites shows similar trends. Important opportunities for further reductions in many carcinogens, including formaldehyde, hexavalent chromium, and a variety of halogenated compounds are identified. Continued work to minimize the use of carcinogens can help to reduce the burden of cancer in Massachusetts and elsewhere.

Environmental and occupational causes of cancer: new evidence 2005-2007.

What do we currently know about the occupational and environmental causes of cancer? As of 2007, the International Agency for Research on Cancer (IARC) identified 415 known or suspected carcinogens. Cancer arises through an extremely complicated web of multiple causes, and we will likely never know the full range of agents or combinations of agents. We do know that preventing exposure to individual carcinogens prevents the disease. Declines in cancer rates-such as the drop in male lung cancer cases from the reduction in tobacco smoking or the drop in bladder cancer among cohorts of dye workers from the elimination of exposure to specific aromatic amines-provides evidence that preventing cancer is possible when we act on what we know. Although the overall age-adjusted cancer incidence rates in the United States among both men and women have declined in the last decade, the rates of several types of cancers are on the rise; some of which are linked to environmental and occupational exposures. This report chronicles the most recent epidemiologic evidence linking occupational and environmental exposures with cancer. Peer-reviewed scientific studies published from January 2005 to June 2007 were reviewed, supplementing our state-of-the-evidence report published in September 2005. Despite weaknesses in certain individual studies, we consider the evidence linking the increased risk of several types of cancer with specific exposures somewhat strengthened by recent publications, among them brain cancer from exposure to non-ionizing radiation, particularly radiofrequency fields emitted by mobile telephones; breast cancer from exposure to the pesticide dichlorodiphenyltrichloroethane (DDT) before puberty; leukemia from exposure to 1,3-butadiene; lung cancer from exposure to air pollution; non-Hodgkin's lymphoma (NHL) from exposure to pesticides and solvents; and prostate cancer from exposure to pesticides, polyaromatic hydrocarbons (PAHs), and metal working fluids or mineral oils. In addition to NHL and prostate cancer, early findings from the National Institutes of Health Agricultural Health Study suggest that several additional cancers may be linked to a variety of pesticides. Our report also briefly describes the toxicological evidence related to the carcinogenic effect of specific chemicals and mechanisms that are difficult to study in humans, namely exposures to bis-phenol A and epigenetic, trans-generational effects. To underscore the multi-factorial, multi-stage nature of cancer, we also present a technical description of cancer causation summarizing current knowledge in molecular biology. We argue for a new cancer prevention paradigm, one based on an understanding that cancer is ultimately caused by multiple interacting factors rather than a paradigm based on dubious attributable fractions. This new cancer prevention paradigm demands that we limit exposure to avoidable environmental and occupational carcinogens, in combination with additional important risk factors like diet and lifestyle. The research literature related to environmental and occupational causes of cancer is constantly growing, and future updates will be carried out in light of new biological understanding of the mechanisms and new methods for studying exposures in human populations. The current state of knowledge is sufficient to compel us to act on what we know. We repeat the call of ecologist Sandra Steingraber: "From the right to know and the duty to inquire flows the obligation to act."