Extensive water damage after major hurricanes and floods increases the likelihood of mold contamination in buildings. This report provides information on how to limit exposure to mold and how to identify and prevent mold-related health effects. Where uncertainties in scientific knowledge exist, practical applications designed to be protective of a person's health are presented. Evidence is included about assessing exposure, clean-up and prevention, personal protective equipment, health effects, and public health strategies and recommendations. The recommendations assume that, in the aftermath of major hurricanes or floods, buildings wet for >48 hours will generally support visible and extensive mold growth and should be remediated, and excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination. Recent parallels to the kind of flooding observed in New Orleans as a result of hurricanes Katrina and Rita occurred in 1997 in Grand Forks, North Dakota, and in 1999 in North Carolina after Hurricane Floyd (2). The number of structures affected was much smaller in North Dakota than in New Orleans, and the population affected in North Carolina was much more dispersed than the population affected in New Orleans. In North Carolina, a reported increase in persons presenting with asthma symptoms was postulated to be caused by exposure to mold (2). In 2001, flooding and subsequent mold growth on the Turtle Mountain reservation in Belcourt, North Dakota was associated with self-reports of rhinitis, rash, headaches, and asthma exacerbation (3). Methods This document was initially prepared by CDC as a guide for public health officials and the general public in response to the massive flooding and the anticipated mold contamination of homes and other structures along the U.S. Gulf Coast associated with hurricanes Katrina and Rita (4). A workgroup was convened of CDC staff with expertise in relevant subject areas. This included medical epidemiologists, environmental epidemiologists and occupational epidemiologists, industrial hygienists, infectious disease physicians and mycologists. The framework for the document was decided by consensus discussions, and workgroup members were assigned to research and to write different sections. The members produced individual written summaries, which formed the basis of the report. Wherever possible, recommendations were based on existing recommendations or guidelines. Where adequate guidelines did not exist, the guidelines were based on CDC experience and expertise.

Several cases of interstitial lung disease have been diagnosed among workers at a nylon flock plant, but the etiologic agent for the disease outbreak was unknown. The results of a medical survey and industrial hygiene study indicated that the dust present in the plant may be responsible. Thus, airborne dust collected at the plant was examined for its inflammatory potential in rat lungs. The endpoints measured were: (1) breathing rates, (2) differential cell counts of bronchoalveolar lavage cells, (3) alveolar macrophage (AM) chemiluminescence, (4) albumin concentration and matrix metalloprotease activities in the acellular fluid from the initial bronchoalveolar lavage, and (5) pulmonary histopathology. In the first study, rats received a single dose of the airborne dust sample (10 mg/kg body weight) by intratracheal (IT) instillation. At 1 d post-IT, all inflammatory endpoints were significantly increased versus controls, but by 29 d post-IT they did not differ significantly from controls. Histopathology demonstrated mild to moderate, multifocal, suppurative pneumonia, usually centered around bronchioles, at 1 d post-IT. At 29 d post-IT, pulmonary inflammation was minimal to mild and characterized by alveolar histocytosis usually restricted to the immediate area of retained bire-fringent fibers. In subsequent experiments, airborne dust was extracted with water and the dust (washed airborne dust) and water extract (soluble fraction) were separated by centrifugation for further study. Nylon tow dust was prepared in the laboratory by milling uncut nylon strands (called tow) that had not been treated with the finish or dyes that are commonly used in the flock plants. Rats were administered a single dose of a dust sample (10 mg/kg body weight) or the soluble fraction (1.3 ml/kg body weight) by IT administration and the same endpoints were measured at 1 d post-IT. The dust samples caused significant increases in all of the inflammatory endpoints; however, the soluble fraction was much less active. Histological analysis of the lungs 1 d post-IT confirmed lung inflammation was occurring and tended to center around bronchioles. The results suggest that: (1) nylon flocking generates particles of respirable size that can interact with AM in the lung and can be detected in the lung 29 d after exposure, (2) the dust samples examined cause an inflammatory response, (3) water-extractable agent(s) from airborne dust contribute only minimally to the inflammatory response, and (4) the acute inflammatory response to these dusts is substantial when compared to other pathologic occupational dusts previously examined in our laboratory.

Background: Molecular tumor boards (MTB) are a key component of most precision oncology programs, designed to provide a structured multidisciplinary approach to evaluating cancer patients (pts) for therapy (Tx), clinical trial (CT) enrollment, and genetic counseling (GC) services. Two health systems separately instituted MTB in 2017, and through a bio-informatics platform have been tracking the impact of these on pt care. We describe the collective experience in tracking MTB impact. Methods: This is a retrospective cohort study of pts reviewed for the first time by MTB between September 1, 2017 and September 30, 2020 at either of the two health systems (HS). Follow up data were obtained by a certified tumor registrar at a median time of 109 days after presentation. Demographics and clinical characteristics of MTB pts were obtained. Pts were identified for whom Tx or CTs were recommended and subsequently administered after MTB review, along with pts for whom GC was recommended and subsequently had genetic testing performed. Results: 351 pts were evaluated. Pt demographics included: median age of 65 years; 61% female; 83% White, 13% Black, 3% Asian, with 2% of Hispanic/Latino ethnicity. The most common primary sites observed were lung (75 pts; 21%), breast (44 pts; 13%) and central nervous system (26 pts, 7%). 334 pts (95%) had data regarding Tx and CT recommendations. 124 pts (37%) received a Tx recommendation and 36 (29%) of these received Tx. 73 pts (22%) received a CT recommendation and 4 (6%) of these pts were enrolled on CTs. 340 pts (97%) had data regarding GC recommendations. 94 pts (28%) received a GC referral and 28 (30%) of these received GC. 25 (89%) of these received a molecular test for germline cancer risk, and 10 (40%) of these had a risk mutation identified in one of the following: ATM (4), BRCA2 (2), BARD1 (1), CHEK2 (1), RAD51C (1), and RET (1). Conclusions: MTB was successful in matching pts to Tx and CT, and in providing appropriate referrals to GC and identifying germline risk mutations. The bio-informatics platform provided a uniform format and structure to collate and analyze data between programs. These parameters will serve as a baseline to monitor future MTB impact and trends as these precision oncology programs continue to grow. The relatively low percentage of patients of color whose cases were reviewed in this MTB analysis merits further understanding. Citation Format: Igor I. Rybkin, Michael A. Thompson, Frank M. Wolf, Kristen Collins, Louisa Laidlaw, Tom Mikkelsen, Jennifer Godden, Mary Walters, James L. Weese, Ronda Broome, Joe Burkhart, Veronica Jones, Chenan Zhang, Thomas D. Brown, Anna Berry. Molecular tumor board impact at two large health systems [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2021 Oct 7-10. Philadelphia (PA): AACR; Mol Cancer Ther 2021;20(12 Suppl):Abstract nr P159.