Non-malignant Respiratory Disease Research Articles

Non-malignant respiratory disease among workers in industries using styrene-A review of the evidence.

Asthma and obliterative bronchiolitis (OB) cases have occurred among styrene-exposed workers. We aimed to investigate styrene as a risk factor for non-malignant respiratory disease (NMRD). From a literature review, we identified case reports and assessed cross-sectional and mortality studies for strength of evidence of positive association (i.e., strong, intermediate, suggestive, none) between styrene exposure and NMRD-related morbidity and mortality. We analyzed 55 articles and two unpublished case reports. Ten OB cases and eight asthma cases were identified. Six (75%) asthma cases had abnormal styrene inhalation challenges. Thirteen (87%) of 15 cross-sectional studies and 12 (50%) of 24 mortality studies provided at least suggestive evidence that styrene was associated with NMRD-related morbidity or mortality. Six (66%) of nine mortality studies assessing chronic obstructive pulmonary disease-related mortality indicated excess mortality. Available evidence suggests styrene exposure is a potential risk factor for NMRD. Additional studies of styrene-exposed workers are warranted. Am. J. Ind. Med. 60:163-180, 2017. © 2016 Wiley Periodicals, Inc.

Palliative Care for Patients with Nonmalignant Respiratory Disease.

Nonmalignant respiratory diseases are chronic and life-limiting conditions that need holistic palliative care. Such patients not only have a variety of physical symptoms such as dyspnea, pain, cough, depression, and anxiety, but also have a number of psychosocial and spiritual issues, which are not addressed to by us. This leads to a poor quality of life. Hence, these patients require supportive palliative care to relieve their sufferings, but unfortunately such care is not available to them in our country. In this article, we have tried to discuss the barriers to the provision of palliative care to such patients and suggested some measures to overcome them.

P2.01-011 Identification of Differentially Expressed Circulating miRNAs in the Serum of NSCLC Patients Using next Generation Sequencing

Aberrant expression of miRNAs has been found in human cancers and has not only been used as diagnostic, prognostic, and predictive biomarkers, but also as potential therapeutic target. In this study, we compared the expression profile of miRNAs in the serum of NSCLC patients with that of non-malignant respiratory disease patients and healthy controls. For this prospective pilot study, a total of 10 subjects were recruited, 2 each of lung adenocarcinoma (ADC), squamous cell carcinoma (SQC), pulmonary tuberculosis (TB), chronic obstructive pulmonary disease (COPD), and healthy controls, from Outpatient Department of Pulmonary Medicine and Sleep Disorders, AIIMS, New Delhi. Approximately 5 ml. of peripheral blood was collected; serum was separated and total RNA was isolated using miRNeasy serum/plasma kit (QIAGEN). Small RNAs were purified from total RNA; libraries of 18 to 50 nt small RNAs were prepared with the TruSeq RNA Library Prep Kit (Illumina), and mature miRNAs were profiled using illumina TruSeq Sequencing Chemistry on illumina HiSeq 2000 next generation sequencing (NGS) platform. Quality check was performed and high quality raw data was mapped on to miRBase database. The expression profile of miRNAs in each subject was analyzed using miRNAkey software and fold change was performed to identify differentially expressed miRNAs in NSCLC as compared to controls. Using NGS, we were able to detect 1074, 1013, 299, 268, and 907 known miRNAs in the serum of lung ADC, SQC, TB, COPD and healthy controls, respectively. A number of miRNAs, such as let-7, miR-10b-5p, miR-15a-5p, miR-23b-5p, miR-92a-3p, miR-148b-3p, miR-185-3p, miR-192-5p, miR-320a, miR-329-3p, miR-342-3p, miR-375, miR-449a, miR-486-5p, miR-497-5p, miR-584-3p, miR-1908-5p, and miR-3195 were found to be downregulated, while miR-10a-5p, miR-148a-3p, and miR-197-3p were found to be upregulated in NSCLC as compared to non-malignant respiratory disease controls and healthy controls (>2 fold change; p<0.05). Further, few miRs, including miR-93-3p, miR-130b-5p, miR-196b-5p, miR-337-3p, miR-378f, miR-382-5p, miR-424-3p, and miR-1271-3p were found to be specifically expressed in NSCLC. A number of miRNAs were found to be dysregulated in the serum of NSCLC patients than controls. The present study is being continued in a larger set of subjects to validate the findings & also the expression patterns of target genes of differentially expressed miRNAs is being analyzed by real-time reverse-transcriptase PCR to find their relevance in lung carcinogenesis. This may prove to be useful for developing non-invasive diagnostic and prognostic tools as well as tools to monitor therapeutic efficacy in NSCLC.

PUB087 Domestic Cooking Fuel as a Risk Factor for Lung Cancer in Women - A Case Control Study

Tobacco smoking is the most common risk factor for lung cancer. But a significant proportion of lung cancer occurs in non-smokers. Indoor pollution due to domestic fuels has been recently implicated as a causative agent in lung cancer especially in women. We conducted a case control study to find out the role of Domestic Cooking Fuel as a risk factor for Lung Cancer in Indian women. In a case control study 67 women with proven lung cancer were recruited. Forty-six females having a non-malignant respiratory disease constituted the control group. The patients and controls were asked about the exposure in various cooking fuels using a questionnaire. There were 50 (74.6%) non-smokers and 17 (25.4%) smokers among the female cancer cases (p=0.016). Adenocarcinoma was the commonest histological type of malignancy (n=26, 38.8%) in the whole group and was the predominant form in the non-smoking females. Tobacco smoking was the most important risk factor for lung cancer with OR of 4.87 (95% CI 1.34-17.76). Among non-smokers out of all the cooking fuels the risk of development of lung cancer was highest for biomass fuel exposure with an odds ratio of 5.33 (95% CI 1.7-16.7).Use of mixed fuels was associated with a lesser risk (OR= 3.04, 95% CI 1.1-8.38). This study indicated that domestic cooking fuel exposure is an important risk factor in the causation of lung cancer among women in addition of exposure to tobacco smoke.

Mortality from respiratory diseases associated with opium use: a population-based cohort study

BackgroundRecent studies have suggested that opium use may increase mortality from cancer and cardiovascular diseases. However, no comprehensive study of opium use and mortality from respiratory diseases has been published....

Reassessing the Link between Airborne Arsenic Exposure among Anaconda Copper Smelter Workers and Multiple Causes of Death Using the Parametric g-Formula.

Background:Prior studies have indicated associations between ingestion of inorganic arsenic and ischemic heart disease, nonmalignant respiratory disease, and lung, skin, bladder, and kidney cancers. In contrast, inhaled arsenic has been consistently associated only with lung cancer. Evidence for health effects of inhaled arsenic derives mainly from occupational studies that are subject to unique biases that may attenuate or obscure such associations.Objectives:We estimated the excess mortality from respiratory cancers, heart disease, and other causes resulting from occupational arsenic exposure while controlling for confounding using the parametric g-formula.Methods:Using a cohort of 8,014 male copper smelter workers who were hired between 1938 and 1955 and followed through 1990, we estimated the impacts of hypothetical workplace interventions on arsenic exposure on the risk of mortality from all causes, heart disease, and lung cancer using the parametric g-formula.Results:We estimate that eliminating arsenic exposure at work would have prevented 22 deaths by age 70 per 1,000 workers [95% confidence interval (CI): 10, 35]. Of those 22 excess deaths, we estimate that 7.2 (95% CI: –1.2, 15) would be due to heart disease, 4.0 (95% CI: –0.8, 8.2) due to respiratory cancers, and 11 (95% CI: 0.0, 23) due to other causes.Conclusions:Our analyses suggest that the excess deaths from causes other than respiratory cancers comprise the majority of the excess deaths caused by inhaled arsenic exposure. Healthy worker survivor bias may have masked such associations in previous analyses. These results emphasize the need for consideration of all exposure routes for upcoming risk assessment by the U.S. Environmental Protection Agency.Citation:Keil AP, Richardson DB. 2017. Reassessing the link between airborne arsenic exposure among Anaconda copper smelter workers and multiple causes of death using the parametric g-formula. Environ Health Perspect 125:608–614; http://dx.doi.org/10.1289/EHP438

Fluoro-edenite induced disease in the Sicilian site of Biancavilla (Italy).

Objectives Fluoro-edenite, a fibrous amphibole present in the soil and building materials of Biancavilla, (Sicily), was allocated in 2014 by the International Agency for Research on Cancer to the Group 1 as cause of mesothelioma. The aim of our research is to monitor the occurrence of mesothelioma and to evaluate data on non-malignant respiratory diseases among Biancavilla residents to better target prevention action. Methods Mesothelioma mortality and pleural cancer hospitalization (2006-2012) as well as incidence data (1998-2003) were analyzed. Standardized Mortality Ratio (SMR), Standardized Hospitalization Ratio (SHR), Standardized Incidence Ratio (SIR) were estimated with respect to regional rates. A descriptive research of the hospitalized pneumoconiosis cases in Biancavilla residents was undertaken (2006-2013). Results A statistically significant death excess from Pleural Mesothelioma (SMR 632) was observed; very high figures and 0.5 sex ratio (M/W) were shown in the younger age groups. Pleural cancer hospitalization showed significant excesses (SHR 399) in particular among younger persons. Mesothelioma incidence was increased in men (SIR 346) and in women (SIR 1221) with a sex ratio equal to one. Twenty-eight cases of pneumoconiosis (18 men and 10 women) were found. Conclusions The study confirms the role of exposure to fluoro-edenite fibres as source of mesothelioma, and the observed sex ratio, regarding mortality, hospitalization and incidence, corroborates the role of an environmental exposure. The higher excesses of death, hospitalizations, and incidence among young subjects suggest early exposure, in teenage/childhood years. The occurrence of unexpected hospitalization for pneumoconiosis in Biancavilla underlines the importance of further investigation on non malignant respiratory diseas

Occupational exposure to cristobalite and mortality from natural causes

Introduction: Occupational exposure to crystalline silica causes lung cancer and non-malignant respiratory disease, but its effects on other outcomes are less clear, which may be due to healthy worker survivor bias. This study re-analyzed a cohort of male diatomaceous earth workers exposed to cristobalite, with special attention to healthy worker survivor bias. Methods: When some workers leave work for health-related reasons, the workers who remain at work accumulate the most occupational exposure and also experience adverse outcomes later. This can result in underestimates of the harmful effects of exposure if proper methods are not used to adjust for time-varying confounding. G-estimation of an accelerated failure time model is well-suited for studying very common outcomes, and allows for correct adjustment for time-varying confounders. Data on occupational exposure to cristobalite was only available through 1994, while follow-up continued through 2011. Exposure was therefore lagged by 17 years. Analysis adjusted for the following confounders: age, Hispanic ethnicity, calendar year, smoking, time off work, previous cumulative exposure to dust, and previous cumulative exposure to asbestos. Preliminary analysis focused on mortality from all natural causes, excluding deaths from external causes. Results: If no one in the cohort had ever been exposed to cristobalite, workers who died of natural causes would have lived an estimated 4.7 (95%CI: 3.1,8.3) years longer, on average. Conclusion: After proper adjustment for healthy worker survivor bias using g-estimation of an accelerated failure time model, cristobalite exposure appears to have led to substantially earlier death from natural causes. Future analyses will consider specific causes and, where appropriate, a truncated follow-up with no lag for exposure.

Tyler asbestos workers: A mortality update in a cohort exposed to amosite

ABSTRACTThe Tyler asbestos plant produced pipe insulation from 1954 to 1972 and exclusively used amosite asbestos. There were 1130 former workers of this plant during the period of operation. A death certificate mortality analysis was published regarding this plant in 1998 for the period through 1993. This study represents an update of the mortality analysis with additional certificates collected for deaths occurring through 2011.Searches of the National Death Index database were conducted in 2004 and again in 2013. At the time of the latter search, only deaths occurring through 2011 were available. In total, 265 distinct additional death certificates were secured and added to 304 available from the original study. After the new certificates were coded (ICD-9), data were analyzed using the Centers for Disease Control and Prevention Life Table Analysis System (LTAS) and standard mortality ratios (SMR) generated with 95% confidence limits (CL). LTAS constructs cause-specific mortality rates by age, gender, race, and person-time at risk, and compares observed rates with a referent population in order to derive SMR. A significant excess number of deaths due to nonmalignant respiratory disease (asbestosis) and from select malignant neoplasms were identified. There were in total 23 mesothelioma deaths (4% of deaths), with 16 pleural and 7 peritoneal. The SMR for malignant neoplasms of the trachea, bronchus, and lung was 244 (with 95% CL 196, 300), suggesting that exposed workers from this cohort were nearly 2.5-fold (244 %) more likely to die from this cause as the general referent population. The analysis also showed that exposures of short duration (<6 mo) produced significantly elevated SMR for all respiratory cancers, lung cancer, and pleural mesothelioma. There was a significant difference in median duration of exposure for mesothelioma types, confirming association of peritoneal mesothelioma with longer duration of exposure. Deaths due to intestinal cancer (predominantly colon; not including rectum) were also found in excess. The mortality experience of the Tyler cohort continues to be followed with great interest, given the exclusivity of exposure to amosite. Data confirm the inherent pathogenicity of this fiber type for nonmalignant disease as well as select cancers, particularly relevant given the importance of this amphibole’s use in the United States.

38P Overall survival in non-smokers and quitters compared to smokers who develop lung cancer: Case–control data from routine clinical practice

recently implicated as a causative agent in lung cancer especially in women. We conducted a case control study to find out the role of Domestic Cooking Fuel as a risk factor for Lung Cancer in Indian women. Methods: In the case control study 67 women with proven lung cancer were recruited. Forty-six females having a non-malignant respiratory disease constituted the control group. The patients and controls were asked about the exposure in various cooking fuels using a questionnaire. Results: There were 50(74.6%) non-smokers and 17(25.4%) smokers among the female cancer cases (p = 0.016). Adenocarcinoma was the commonest histological type of malignancy (n = 26, 38.8%) in the whole group and was the predominant form in the non-smoking females. Tobacco smoking was the most important risk factor for lung cancer with OR of 4.87 (95% CI 1.34–17.76). Among non-smokers out of all the cooking fuels the risk of development of lung cancer was highest for biomass fuel exposure with an odds ratio of 5.33 (95% CI 1.7–16.7). Use of mixed fuels was associated with a lesser risk (OR=3.04, 95% CI 1.1–8.38). Conclusions: This study indicated that domestic cooking fuel exposure is an important risk factor in the causation of lung cancer among women in addition of exposure to tobacco smoke. Legal entity responsible for the study: PSM Dental College and Hospital Funding: PSM Dental College and Hospital Disclosure: All authors have declared no conflicts of interest.

Mortality from asbestos-associated disease in Libby, Montana 1979\u20132011

Research on asbestos exposure in Libby, MT, has focused on occupational exposure in vermiculite mining and processing, but less attention has been paid to asbestos-related mortality among community members without vermiculite mining occupational history. Our study reports on asbestos-related mortality in Libby over 33 years (1979–2011) while controlling for occupational exposure. We calculated sex-specific 33-year standardized mortality ratios (SMRs) for Libby residents who died from 1979 to 2011 with an asbestos-related cause of death. Decedent address at time of death was geocoded to confirm inclusion in the Libby County Division. We controlled for past W.R. Grace employment by including and then removing them from the SMR analysis. Six hundred and ninety-four decedents were identified as having at least one asbestos-related cause of death and residing in our study area boundary. Statistically significant (P<0.05) 33-year SMRs, both before and after controlling for W.R. Grace employment, were found for: male and female non-malignant respiratory diseases, female COPD, and asbestosis for both sexes combined. Eighty-five men and two women were matched to employment records. We observed elevated asbestos-related mortality rates among males and females. SMR results for asbestosis were high for both sexes, even after controlling for past W.R. Grace employment. These results suggest that the general population may be experiencing asbestos-related effects, not just former vermiculite workers. Additional research is needed to determine whether SMRs remain elevated after controlling for secondary exposure, such as living with vermiculite workers.

Increased Lung Cancer Mortality in Taconite Mining: The Potential for Disease from Elongate Mineral Particle Exposure.

Taconite mining involves potential exposure to non-asbestiform amphibole mineral fiber. More recent studies have demonstrated increased mortality from respiratory cancers and heart disease among workers in the taconite industry. This finding is not consistent with recent exposure assessment findings, nor is the toxicology of this mineral suggestive of neoplastic disease. The understanding of respiratory disease in taconite mining is hampered by the lack of exposure data to asbestiform mineral fibers that occurred in the 1950s and 1960s. Other industries with similar mineral exposure have not demonstrated definitive associations with respiratory cancer, although non-malignant respiratory disease is a consistent finding in epidemiological studies.

Respiratory Cancer and Non-Malignant Respiratory Disease-Related Mortality among Older Construction Workers-Findings from the Health and Retirement Study.

ObjectiveThis study explored the risk of respiratory cancer and non-malignant respiratory disease (NMRD)-related mortality among older construction workers.MethodsAnalyzed data from the 1992–2010 RAND Health and Retirement Study (HRS) and the HRS National Death Index – Cause of Death file. About 25,183 workers aged 50 years and older were examined, including 5,447 decedents and 19,736 survivors, of which 1,460 reported their longest job was in construction. Multinomial logistic regression assessed the differences in mortality between workers’ longest occupations, controlling for confounders.ResultsAfter adjusting for smoking and demographics, construction workers were almost twice as likely to die from respiratory cancer (OR = 1.65; CI: 1.10–2.47) or NMRD (OR = 1.73; CI: 1.16–2.58) compared to white-collar workers.ConclusionsThis study adds to the growing evidence that respiratory cancer and NMRD are frequently associated with construction exposure.

Persistent effects of Libby amphibole and amosite asbestos following subchronic inhalation in rats.

BackgroundHuman exposure to Libby amphibole (LA) asbestos increases risk of lung cancer, mesothelioma, and non-malignant respiratory disease. This study evaluated potency and time-course effects of LA and positive control amosite (AM) asbestos fibers in male F344 rats following nose-only inhalation exposure.MethodsRats were exposed to air, LA (0.5, 3.5, or 25.0 mg/m3 targets), or AM (3.5 mg/m3 target) for 10 days and assessed for markers of lung inflammation, injury, and cell proliferation. Short-term results guided concentration levels for a stop-exposure study in which rats were exposed to air, LA (1.0, 3.3, or 10.0 mg/m3), or AM (3.3 mg/m3) 6 h/day, 5 days/week for 13 weeks, and assessed 1 day, 1, 3, and 18 months post-exposure. Fibers were relatively short; for 10 mg/m3 LA, mean length of all structures was 3.7 μm and 1 % were longer than 20 μm.ResultsTen days exposure to 25.0 mg/m3 LA resulted in significantly increased lung inflammation, fibrosis, bronchiolar epithelial cell proliferation and hyperplasia, and inflammatory cytokine gene expression compared to air. Exposure to 3.5 mg/m3 LA resulted in modestly higher markers of acute lung injury and inflammation compared to AM. Following 13 weeks exposure, lung fiber burdens correlated with exposure mass concentrations, declining gradually over 18 months. LA (3.3 and 10.0 mg/m3) and AM produced significantly higher bronchoalveolar lavage markers of inflammation and lung tissue cytokines, Akt, and MAPK/ERK pathway components compared to air control from 1 day to 3 months post-exposure. Histopathology showed alveolar inflammation and interstitial fibrosis in all fiber-exposed groups up to 18 months post-exposure. Positive dose trends for incidence of alveolar epithelial hyperplasia and bronchiolar/alveolar adenoma or carcinoma were observed among LA groups.ConclusionsInhalation of relatively short LA fibers produced inflammatory, fibrogenic, and tumorigenic effects in rats which replicate essential attributes of asbestos-related disease in exposed humans. Fiber burden, inflammation, and activation of growth factor pathways may persist and contribute to lung tumorigenesis long after initial LA exposure. Fiber burden data are being used to develop a dosimetry model for LA fibers, which may provide insights on mode of action for hazard assessment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0130-z) contains supplementary material, which is available to authorized users.

Exercise training to improve exercise capacity and quality of life in people with non-malignant dust-related respiratory diseases.

Non-malignant dust-related respiratory diseases, such as asbestosis and silicosis, are similar to other chronic respiratory diseases and may be characterised by breathlessness, reduced exercise capacity and reduced health-related quality of life. Some non-malignant dust-related respiratory diseases are a global health issue and very few treatment options, including pharmacological, are available. Therefore, examining the role of exercise training is particularly important to determine whether exercise training is an effective treatment option in non-malignant dust-related respiratory diseases. To assess the effects of exercise training for people with non-malignant dust-related respiratory diseases compared with control, placebo or another non-exercise intervention on exercise capacity, health-related quality of life and levels of physical activity. We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE/PubMed, EMBASE, CINAHL, PEDro and AMED (all searched from inception until February 2015), national and international clinical trial registries, reference lists of relevant papers and we contacted experts in the field for identification of suitable studies. We included only randomised controlled trials (RCTs) that compared exercise training of at least four weeks duration with no exercise training, placebo or another non-exercise intervention. We used standard methodological procedures expected by Cochrane. Two review authors independently assessed study eligibility and risk of bias, and extracted data. We employed the GRADE approach to assess the overall quality of evidence for each outcome and to interpret findings. We synthesized study results using a random-effects model based on the assessment of heterogeneity. We conducted subgroup analyses on participants with dust-related interstitial lung diseases (ILDs) and participants with asbestos related pleural disease (ARPD). Two RCTs including a combined total of 40 participants (35 from one study and five from a second study) met the inclusion criteria. Twenty-one participants were randomised to the exercise training group and 19 participants were randomised to the control group. The included studies evaluated the effects of exercise training compared to a control group of no exercise training in people with dust-related ILDs and ARPD. The exercise training programme in both studies was in an outpatient setting for an eight-week period. The risk of bias was low in both studies. There were no reported adverse events of exercise training. Following exercise training, six-minute walk distance (6MWD) increased with a mean difference (MD) of 53.81 metres (m) (95% CI 34.36 to 73.26 m). Improvements were also seen in the domains of health-related quality of life: Chronic Respiratory Disease Questionnaire (CRQ) Dyspnoea domain (MD 2.58, 95% CI 0.72 to 4.44); CRQ Fatigue domain (MD 1.00, 95% CI 0.11 to 1.89); CRQ Emotional Function domain (MD 2.61, 95% CI 0.74 to 4.49); and CRQ Mastery domain (MD 1.51, 95% CI 0.29 to 2.72). Improvements in exercise capacity and health-related quality of life were also evident six months following the intervention period: 6MWD (MD 52.68 m, 95% CI 27.43 to 77.93 m); CRQ Dyspnoea domain (MD 3.03, 95% CI 1.41 to 4.66); CRQ Emotional Function domain (MD 5.57, 95% CI 2.34 to 8.81); and CRQ Mastery domain (MD 2.66, 95% CI 1.08 to 4.23). Exercise training did not result in improvements in the Modified Medical Research Council (MMRC) dyspnoea scale immediately following exercise training or six months following exercise training. The improvements following exercise training were similar in a subgroup of participants with dust-related ILDs and in a subgroup of participants with ARPD compared to the control group, with no statistically significant differences in treatment effects between the subgroups. The evidence examining exercise training in people with non-malignant dust-related respiratory diseases is of very low quality. This is due to imprecision in the results from the small number of trials and the small number of participants, the indirectness of evidence due to a paucity of information on disease severity and the data from one study being from a subgroup of participants, and inconsistency from high heterogeneity in some results. Therefore, although the review findings indicate that an exercise training programme is effective in improving exercise capacity and health-related quality of life in the short-term and at six months follow-up, we remain unsure of these findings due to the very low quality evidence. Larger, high quality trials are needed to determine the strength of these findings.

Cohort Study of Carbon Black Exposure and Risk of Malignant and Nonmalignant Respiratory Disease Mortality in the US Carbon Black Industry.

To evaluate lung cancer and respiratory disease mortality associations with cumulative inhalable carbon black exposure among 6634 US carbon black workers. This analysis was performed using standardized mortality ratio (SMRs) and Cox regression analyses. Lung cancer mortality was decreased overall (SMR = 0.77; 95% confidence interval [CI], 0.67 to 0.89) but less so among hourly male workers (SMR = 0.87; 95% CI, 0.71 to 1.05). No exposure-response association was observed with time-dependent cumulative inhalable carbon black: hazard ratio [HR] = 1.0 (95% CI, 0.6 to 1.6) for 20 to less than 50 mg/m·yr); HR = 1.3 (95% CI, 0.8 to 2.1) for 50 to less than 100 mg/m·yr; and HR = 1.4 (95% CI, 0.9 to 2.1) for 100 mg/m·yr or more compared with referent (<20 mg/m·yr). No consistent associations were observed between cumulative inhalable carbon black exposure and respiratory disease mortality. Quantitative carbon black exposure estimates were not related to lung cancer or nonmalignant respiratory disease mortality.

Arsenic Exposure And Nonmalignant Respiratory Disease: A Systematic Review Of The Epidemiological Evidence

Introduction: Arsenic (As) exposure via inhalation and ingestion are known causes of lung cancer. However the body of epidemiological research on As and nonmalignant respiratory disease is less coh...

Associations Between Long-Term Exposure To Air Pollution And Perturbations In The Transcriptome

Epidemiologic studies have consistently shown associations between long-term exposure to ambient air pollution and chronic health effects such as cardiovascular disease, non-malignant respiratory disease, and lung cancer. We hypothesized that early indications of biological perturbations due to ambient air pollution could be detected in genome-wide gene expression profiles from peripheral blood mononuclear cells (PBMC) in healthy individuals. We assessed genome-wide gene expression in PBMC samples from study participants of two prospective cohorts from Italy (n=95) and Sweden (n=455). We estimated long-term air pollution (NOx) exposure levels for our study participants using exposure models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). We used three complementary statistical approaches: univariate analysis (coupled with a 5% false discovery rate (FDR) control to account for multiple testing), elastic net regression, and Graphical Unit Evolutionary Stochastic Search (GUESS; a recent Bayesian variable selection approach), to identify for which genes expression level was altered by long-term exposure to NOx. There was little overlap between the distribution of NOx exposure levels in the Italian and the Swedish cohort (median; 5th-95th percentile: 94.2; 7.8-124.6 and 6.7; 4.8-19.5 μg/m3, respectively). We therefore conducted our primary analyses in the two cohorts separately. Using the univariate approach we identified one (unannotated) transcript in the Italian cohort and no transcripts in the Swedish cohort that were significantly associated at an FDR of 5%. While elastic net regression provided consistent results, GUESS provided less indication for an association with this probe in the Italian data. In summary, our study does not provide strong indications of transcriptomic changes related to air pollution within the exposure range studied.

Modelling the health risks of exposure to respirable crystalline silica from hydraulic fracturing operations in the USA shale plays

Respirable crystalline silica (RCS) is a known human carcinogen and a contaminant of potential concern. Proppants are used during the process of well stimulation (hydraulic fracturing) as additives in the fluid cocktail and sand is often used as a proppant which contains high percentage of silica determined by the quartz content. Empirical occupational exposure risk models were employed in this study to assess the potential health consequences from chronic RCS exposures based on RCS data from NIOSH and risk assessment formulas. Evaluating the lifetime (LT) excess cancer risk (LCR) potential, based on a risk target of 105, the job titles that are likely to experience any substantial potential effect of cancer induction are the sand mover (LCR = 16.1 × 105) and transfer belt (LCR = 19.2 × 105) operators. The sand truck driver and data Van operators are among the job functions with a cumulative disease burden of 7.2% that are unlikely to be affected by &lt; 2% carcinogenic disease burden. The chemical truck, sand mover and transfer belt (T-belt) operators may potentially be at risk of other occupational nonmalignant respiratory diseases with hazard quotient (HQ) of 0.65, 1.79, and 2.13 respectively. It is recommended that continuous occupational health monitoring of potentially exposed workers should be included as part of the project plan and the engineering risk controls that have been put in place should be ranked to highlight the effectiveness of any risk reduction/prevention methodology employed.

Palliative care for patients with non-malignant respiratory disease

Non-malignant respiratory disease is a chronic life-limiting condition that requires holistic palliative care. Patients with non-malignant respiratory disease have a range of biopsychosocial and spiritual needs, which healthcare professionals should recognise and manage effectively. Healthcare professionals have an important role in enabling the delivery of effective palliative care to this group of patients and their carers, and in recognising the many factors that may impede delivery of palliative care.