BackgroundThousands of rescue and recovery workers descended on the World Trade Center (WTC) in the wake of the terrorist attack of September 11, 2001 (9/11). Recent studies show that respiratory illness and post-traumatic stress disorder (PTSD) are the hallmark health problems, but relationships between them are poorly understood. The current study examined this link and evaluated contributions of WTC exposures.MethodParticipants were 8508 police and 12 333 non-traditional responders examined at the WTC Medical Monitoring and Treatment Program (WTC-MMTP), a clinic network in the New York area established by the National Institute for Occupational Safety and Health (NIOSH). We used structural equation modeling (SEM) to explore patterns of association among exposures, other risk factors, probable WTC-related PTSD [based on the PTSD Checklist (PCL)], physician-assessed respiratory symptoms arising after 9/11 and present at examination, and abnormal pulmonary functioning defined by low forced vital capacity (FVC).ResultsFewer police than non-traditional responders had probable PTSD (5.9% v. 23.0%) and respiratory symptoms (22.5% v. 28.4%), whereas pulmonary function was similar. PTSD and respiratory symptoms were moderately correlated (r=0.28 for police and 0.27 for non-traditional responders). Exposure was more strongly associated with respiratory symptoms than with PTSD or lung function. The SEM model that best fit the data in both groups suggested that PTSD statistically mediated the association of exposure with respiratory symptoms.ConclusionsAlthough longitudinal data are needed to confirm the mediation hypothesis, the link between PTSD and respiratory symptoms is noteworthy and calls for further investigation. The findings also support the value of integrated medical and psychiatric treatment for disaster responders.

There are compelling reasons to conduct studies of cancer in Hispanics, the fastest growing major demographic group in the United States (from 15% to 30% of the U.S. population by 2050). The genetically admixed Hispanic population coupled with secular trends in environmental exposures and lifestyle/behavioral practices that are associated with immigration and acculturation offer opportunities for elucidating the effects of genetics, environment, and lifestyle on cancer risk and identifying novel risk factors. For example, traditional breast cancer risk factors explain less of the breast cancer risk in Hispanics than in non-Hispanic whites (NHW), and there is a substantially greater proportion of never-smokers with lung cancer in Hispanics than in NHW. Hispanics have higher incidence rates for cancers of the cervix, stomach, liver, and gall bladder than NHW. With respect to these cancers, there are intriguing patterns that warrant study (e.g., depending on country of origin, the five-fold difference in gastric cancer rates for Hispanic men but not Hispanic women). Also, despite a substantially higher incidence rate and increasing secular trend for liver cancer in Hispanics, there have been no studies of Hispanics reported to date. We review the literature and discuss study design options and features that should be considered in future studies.

These analyses provide further evidence that PTSD is a risk factor for respiratory symptoms and are consistent with evidence implicating physiological dysregulation associated with PTSD in the development of medical conditions. If these effects are verified experimentally, treatment of PTSD may prove helpful in managing physical and mental health of disaster responders.

No abstract

The endothelin pathway plays a critical role in melanoma tumor progression by a variety of mechanisms that enhance tumor cell growth, invasion, and metastasis. Here, we investigate the effect of this pathway on CXC chemokine expression in human melanoma cells and melanocytes. As determined by ELISA, endothelin-1 (ET-1) induces CXCL1 and CXCL8 secretion in three human melanoma cell lines in a concentration-dependent fashion. These responses are mediated by the endothelin-B receptor and are sustained over a 40 h time course. ET-1 does not induce CXCL1 secretion in primary human melanocytes but ET-3, an endothelin isoform, induces a low level of CXCL1 secretion in certain cultures. Neither ET-1 nor ET-3 induces secretion of CXCL8 in primary human melanocytes; thus, this response may be specific for melanocytic cells that have undergone malignant transformation. We have previously demonstrated that ET-1 induces changes in the expression of adhesion molecules in melanoma cells such that invasion and metastasis are favored. This study demonstrates that ET-1 additionally induces secretion of CXC chemokines critical for melanoma metastasis and tumor progression.

WEAS is prevalent in this urban minority population.

Frequency dependence of compliance (FDC) reflects non-homogeneous ventilatory distribution and, in the presence of a normal measured airway resistance, suggests peripheral airways dysfunction. This study evaluated peripheral airway function and bronchial reactivity in irritant exposed or non-exposed individuals with normal routine pulmonary function tests (PFTs) who had persistent unexplained lower respiratory symptoms. Twenty-two patients were identified with persistent respiratory symptoms and with normal chest X-ray and PFTs. Twenty were non-smokers; two had stopped smoking more than 10 years before evaluation. Twelve patients had been exposed to irritants in their workplaces or at home. Non-specific bronchial hyper-reactivity (nsBHR) and FDC, pre- and post-bronchodilator, were measured in all patients. Studies were repeated in 6/12 irritant-exposed subjects after exposure removal and inhaled corticosteroid treatment. Whereas 12/22 patients had nsBHR, all 22 subjects demonstrated FDC [dynamic lung compliance/static lung compliance Cdyn,1 / Cst,1 at respiratory frequency 60 min(-1) (f60), mean 46%, range 27-67%]. After bronchodilator administration, a 15% improvement Cdyn,1 was observed most consistently at f60 (mean% improvement 26%, 95% CI 14-38%) and in subjects without nsBHR. However, Cdyn,1 at f60 did not return to normal after inhaled bronchodilator. Irritant-exposed and unexposed individuals appeared similar in results of testing for FDC and nsBHR. FDC and its response to bronchodilators provide objective physiological measures of an airway abnormality which may provide a basis for clinical symptoms in patients with normal routine pulmonary function studies. The presence of persistently abnormal FDC after bronchodilator (BD) and on follow up studies may reflect chronic inflammatory and/or structural changes in the airways in addition to bronchoconstriction.

Occupational asthma (OA) and work-exacerbated asthma (WEA), collectively known as work-related asthma (WRA), have been recognized as the most prevalent work-related lung diseases in the industrialized world. OA is asthma caused by workplace conditions, and is subdivided into sensitizer-induced (allergic) OA and irritant-induced (nonallergic) OA. WEA is asthma that is made worse, but was not initially caused, by workplace conditions. Although WRA is rarely fatal, patients with WRA frequently experience excessive time lost from work, workplace-specific severe disability, loss of income, job loss, and related psychosocial and financial problems. More than 400 workplace environmental agents have been reported to cause WRA, and are classified by molecular weight and allergenic and irritant properties. Diagnosis of WRA requires confirmation of a diagnosis of asthma plus evidence that the asthma was caused or worsened by workplace conditions. Accuracy of diagnosis is important because either overdiagnosis or missed diagnosis of WRA can be problematic for the patient. Self-reported clinical symptoms alone have only fair sensitivity and specificity for OA. If possible, diagnostic assessment should also include objective evidence with functional and immunologic testing. Treatment and prevention of onset or worsening of WRA can be highly effective and typically include both optimal medical management (generally the same as for non-WRA) and, importantly, avoidance of sensitizer or irritant exposures that caused or exacerbate the asthma. In most cases of OA, prognosis is better with cessation rather than reduction of exposure, and this may require substantial changes in the workplace environment or change of job or even profession.