Mena Kristina D, Gerba Charles P
University of Texas, Houston School of Public Health, Houston, Texas, USA.
Rev Environ Contam Toxicol. 2009;198:133-67. doi: 10.1007/978-0-387-09647-6_4.
Adenoviruses are associated with numerous disease outbreaks, particularly those involving d-cares, schools, children's camps, hospitals and other health care centers, and military settings. In addition, adenoviruses have been responsible for many recreational water outbreaks, including a great number of swimming pool outbreaks than any other waterborne virus (Gerba and Enriquez 1997). Two drinking water outbreaks have been documented for adenovirus (Divizia et al. 2004; Kukkula et al. 1997) but none for food. Of the 51 known adenovirus serotypes, one third are associated with human disease, while other infections are asymptomatic. Human disease associated with adenovirus infections include gastroenteritis, respiratory infections, eye infections, acute hemorrhagic cystitis, and meningoencephalitis (Table 2). Children and the immunocompromised are more severely impacted by adenovirus infections. Subsequently, adenovirus is included in the EPA's Drinking Water Contaminant Candidate List (CCL), which is a list of unregulated contaminants found in public water systems that may pose a risk to public health (National Research Council 1999). Adenoviruses have been detected in various waters worldwide including wastewater, river water, oceans, and swimming pools (Hurst et al. 1988; Irving and Smith 1981; Pina et al. 1998). Adenoviruses typically outnumber the enteroviruses, when both are detected in surface waters. Chapron et al. (2000) found that 38% of 29 surface water samples were positive for infectious Ad40 and Ad41. Data are lacking regarding the occurrence of adenovirus in water in the US, particularly for groundwater and drinking water. Studies have shown, however, that adenoviruses survive longer in water than enteroviruses and hepatitis A virus (Enriquez et al. 1995), which may be due to their double-stranded DNA. Risk assessments have been conducted on waterborne adenovirus (Crabtree et al. 1997; van Heerden et al. 2005c). Using dose-response data for inhalation from Couch et al. (1966), human health risks of infection, illness and death have been determined for various adenovirus exposures. Crabtree et al. (1997) conclude that, even at an adenovirus concentration of 1 per 1,000 L of drinking water, annual risks of infection exceed the suggested risk recommendation of 1 x 10(-4) per yr (Regli et al. 1991) (Table 8). Using the same exposure and dose-response assumptions, van Heerden et al. (2005c) determined annual risks of infection to be 1-1.7 x 10(-1) for two drinking water samples from South Africa containing 1.40 and 2.45 adenoviruses per 10,000 L, respectively. This present study estimated annual risks of infection associated with varying levels of adenoviruses per 100 L (Table 9). By assuming a 2 L/d exposure and utilizing the exponential model at r = 0.4172 (Haas et al. 1993), yearly risks exceed the risk recommendation of 1 x 10(-4) at every exposure level. There are limited data regarding the removal of adenoviruses by conventional water treatment or other physical-chemical treatment processes, but studies do suggest that adenoviruses are of equal or greater sensitivity to oxidizing disinfectants, when compared to waterborne viruses (the most resistant to ultraviolet light). Data suggest that the chlorine doses applied to control other waterborne viruses are more effective against adenovirus, resulting in a greater than 4-log10 removal of adenoviruses by conventional treatment and chlorination. If treatment can achieve a 4-log10 removal of adenoviruses, then, based on the risk levels presented in Table 9, surface water concentrations should not exceed 0.5 adenoviruses per 100 L (Fig. 2). More data are needed regarding effectiveness of water treatment against adenovirus and the human-virus dose-response relationship to fully understand the role of adenovirus as a waterborne public health threat.
腺病毒与众多疾病暴发相关,尤其是那些涉及日托中心、学校、儿童营地、医院及其他医疗保健中心以及军事场所的疾病暴发。此外,腺病毒还导致了许多与娱乐用水相关的疾病暴发,包括比其他任何水源性病毒都多的游泳池疾病暴发(Gerba和Enriquez,1997年)。已记录到两起由腺病毒引起的饮用水疾病暴发(Divizia等人,2004年;Kukkula等人,1997年),但未记录到由食物引起的暴发。在已知的51种腺病毒血清型中,三分之一与人类疾病相关,而其他感染则无症状。与腺病毒感染相关的人类疾病包括肠胃炎、呼吸道感染、眼部感染、急性出血性膀胱炎和脑膜脑炎(表2)。儿童和免疫功能低下者受腺病毒感染的影响更为严重。随后,腺病毒被列入美国环境保护局(EPA)的饮用水污染物候选名单(CCL),该名单列出了公共供水系统中发现的可能对公众健康构成风险的未受监管污染物(国家研究委员会,1999年)。在全球各地的各种水体中都检测到了腺病毒,包括废水、河水、海洋和游泳池(Hurst等人,1988年;Irving和Smith,1981年;Pina等人,1998年)。当在地表水中同时检测到腺病毒和肠道病毒时,腺病毒的数量通常超过肠道病毒。Chapron等人(2000年)发现,29个地表水样本中有38%的样本Ad40和Ad41感染性呈阳性。关于美国水体中腺病毒的发生情况,尤其是地下水和饮用水中的情况,数据匮乏。然而,研究表明,腺病毒在水中的存活时间比肠道病毒和甲型肝炎病毒更长(Enriquez等人,1995年),这可能是由于它们的双链DNA所致。已对水源性腺病毒进行了风险评估(Crabtree等人,1997年;van Heerden等人,2005c)。利用Couch等人(1966年)吸入的剂量反应数据,确定了各种腺病毒暴露情况下的人类感染、患病和死亡的健康风险。Crabtree等人(1997年)得出结论,即使饮用水中腺病毒浓度为每1000升1个,每年的感染风险也超过了建议的风险推荐值1×10⁻⁴/年(Regli等人,1991年)(表8)。使用相同的暴露和剂量反应假设,van Heerden等人(2005c)确定,来自南非的两个饮用水样本中,每10000升分别含有1.40和2.45个腺病毒,每年的感染风险为1 - 1.×10⁻¹。本研究估计了每100升中不同腺病毒水平相关的每年感染风险(表9)。通过假设每天暴露2升,并利用r = 0.4172时的指数模型(Haas等人,1993年),在每个暴露水平下,每年的风险都超过了1×10⁻⁴的风险推荐值。关于传统水处理或其他物理化学处理过程对腺病毒的去除情况,数据有限,但研究确实表明,与水源性病毒(对紫外线最具抵抗力)相比,腺病毒对氧化消毒剂的敏感性相同或更高。数据表明,用于控制其他水源性病毒的氯剂量对腺病毒更有效,通过传统处理和氯化可实现对腺病毒大于4个对数级的去除。如果处理能够实现对腺病毒4个对数级的去除,那么根据表9中的风险水平,地表水浓度不应超过每100升0.5个腺病毒(图2)。需要更多关于水处理对腺病毒的有效性以及人 - 病毒剂量反应关系的数据,以充分了解腺病毒作为水源性公共卫生威胁的作用。