title: Health and environmental consequences of the world trade center disaster.
abstract: The attack on the World Trade Center (WTC) created an acute environmental disaster of enormous magnitude. This study characterizes the environmental exposures resulting from destruction of the WTC and assesses their effects on health. Methods include ambient air sampling; analyses of outdoor and indoor settled dust; high-altitude imaging and modeling of the atmospheric plume; inhalation studies of WTC dust in mice; and clinical examinations, community surveys, and prospective epidemiologic studies of exposed populations. WTC dust was found to consist predominantly (95%) of coarse particles and contained pulverized cement, glass fibers, asbestos, lead, polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and polychlorinated furans and dioxins. Airborne particulate levels were highest immediately after the attack and declined thereafter. Particulate levels decreased sharply with distance from the WTC. Dust pH was highly alkaline (pH 9.0-11.0). Mice exposed to WTC dust showed only moderate pulmonary inflammation but marked bronchial hyperreactivity. Evaluation of 10,116 firefighters showed exposure-related increases in cough and bronchial hyperreactivity. Evaluation of 183 cleanup workers showed new-onset cough (33%), wheeze (18%), and phlegm production (24%). Increased frequency of new-onset cough, wheeze, and shortness of breath were also observed in community residents. Follow-up of 182 pregnant women who were either inside or near the WTC on 11 September showed a 2-fold increase in small-for-gestational-age (SGA) infants. In summary, environmental exposures after the WTC disaster were associated with significant adverse effects on health. The high alkalinity of WTC dust produced bronchial hyperreactivity, persistent cough, and increased risk of asthma. Plausible causes of the observed increase in SGA infants include maternal exposures to PAH and particulates. Future risk of mesothelioma may be increased, particularly among workers and volunteers exposed occupationally to asbestos. Continuing follow-up of all exposed populations is required to document the long-term consequences of the disaster.
authors.affiliation: Mount Sinai School of Medicine, New York, New York 10029, USA. phil.landrigan@mssm.edu
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Landrigan
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Lioy
authors.forename: George
authors.initials: G
authors.lastname: Thurston
authors.forename: Gertrud
authors.initials: G
authors.lastname: Berkowitz
authors.forename: L C
authors.initials: LC
authors.lastname: Chen
authors.forename: Steven N
authors.initials: SN
authors.lastname: Chillrud
authors.forename: Stephen H
authors.initials: SH
authors.lastname: Gavett
authors.forename: Panos G
authors.initials: PG
authors.lastname: Georgopoulos
authors.forename: Alison S
authors.initials: AS
authors.lastname: Geyh
authors.forename: Stephen
authors.initials: S
authors.lastname: Levin
authors.forename: Frederica
authors.initials: F
authors.lastname: Perera
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Rappaport
authors.forename: Christopher
authors.initials: C
authors.lastname: Small
mesh_terms: D000328:Adult; D000401:Aircraft; D000818:Animals; D003252:Construction Materials; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D015994:Incidence; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D008168:Lung / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008875:Middle Aged; D009519:New York City; D016273:Occupational Exposure; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis / Q000506:poisoning; D011247:Pregnancy; D015995:Prevalence; D012140:Respiratory Tract Diseases / Q000453:epidemiology / Q000209:etiology*; D018570:Risk Assessment; D023481:Terrorism
chemical_list: D011084:Polycyclic Aromatic Hydrocarbons