port were collected quarterly from an online database of ate laws, analyzed using a coding scheme and decision les, and transferred into the STATE System database. The TATE System tracks state smoking restrictions in govern

ent worksites, private-sector worksites, restaurants, bars, >mmercial and home-based child care centers, and other ttings, including shopping malls, grocery stores, enclosed enas, public transportation, hospitals, prisons, and ɔtels and motels. Tobacco-control personnel in state health partments reviewed and verified the coding of smoking strictions in their states.

This study did not include laws that were enacted or :came effective after December 31, 2007. For example, inois and Maryland enacted smoking restrictions in 2007 at went into effect in early 2008, and were therefore not cluded in this study.

During December 31, 2004-December 31, 2007, based 1 the effective date of state laws (i.e., the date that these ws actually took effect, not the date they were enacted) d the STATE System coding scheme, the level of smokg restrictions became more protective for private-sector orksites in 18 states, for restaurants in 18 states, and for rs in 12 states. No states relaxed their smoking restric›ns in any of these three settings during the study period. addition, the number of states requiring private-sector orksites to be smoke-free increased from five to 22. As of ecember 31, 2004, Delaware, Florida, Massachusetts, ew York, and South Dakota had banned smoking in prite-sector worksites. As of December 31, 2007, an addiɔnal 17 states (Arizona, Arkansas, Colorado, DC, Hawaii, >uisiana, Minnesota, Montana, Nevada, New Jersey, New exico, North Dakota, Ohio, Rhode Island, Tennessee, tah, and Washington) had done so. During the study riod, the number of states with no smoking restrictions place for private-sector worksites decreased from 24 to

During the 3 years ending December 31, 2007, the numr of states requiring restaurants to be smoke-free increased om seven to 21. By the end of 2004, Delaware, Florida, aho, Maine, Massachusetts, New York, and Utah had nned smoking in restaurants. As of December 31, 2007, additional states (Arizona, Colorado, DC, Hawaii, Louina, Minnesota, Montana, Nevada, New Hampshire, New sey, Ohio, Rhode Island, Tennessee, and Washington) d done so. During this same period, the number of states th no smoking restrictions for restaurants decreased from 1 to nine.

During the same 3-year period, the number of states requiring bars to be smoke-free increased from four to 13. By the end of 2004, Delaware, Maine, Massachusetts, and New York had banned smoking in bars. As of December 31, 2007, an additional nine states (Arizona, Colorado, DC, Hawaii, Minnesota, New Jersey, Ohio, Rhode Island, and Washington) had done so. During the 3 years of this study, the number of states with no smoking restrictions for bars decreased from 43 to 31.

From December 31, 2004 to December 31, 2007, the number of states requiring all three venues included in this study to be smoke-free increased from three to 12. By the end of 2004, Delaware, Massachusetts, and New York had banned smoking in all three settings. As of December 31, 2007, Arizona, Colorado, DC, Hawaii, Minnesota, New Jersey, Ohio, Rhode Island, and Washington also had implemented such comprehensive laws. During the study period, the number of states with smoke-free provisions in place in at least one of the three settings included in this study increased from eight to 25. During this same period, the number of states without any smoking restrictions in place for any of these settings decreased from 16 to eight. Reported by: M Tynan, Maya Tech Corporation, Silver Spring, Maryland. S Babb, MPH, A MacNeil, MPH, Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, CDC. Editorial Note: The findings of this analysis indicate that the number and restrictiveness of state laws regulating smoking in private-sector worksites, restaurants, and bars increased substantially from December 31, 2004, to December 31, 2007. This increase has provided U.S. nonsmokers with increased protection from SHS exposure and its health effects (1).

As of 2003, the most recent data available, 77% of U.S. indoor workers aged ≥18 years reported that their workplace had an official policy that prohibited smoking in indoor work areas and public or common areas (5), compared with 47% during 1992-1993 (1). However, the proportion of workers covered by such policies varied by occupation. In 2003, for example, 83% of white collar workers reported working under a smoke-free workplace policy, compared with 75% of service workers, 63% of blue collar workers, and 72% of food-service workers (5). As a result of continuing gaps and disparities in policy coverage for many private-sector worksites, restaurants, and bars, millions of U.S. nonsmokers continue to be exposed to SHS and its health effects in these settings, either as employees or as patrons.

Smoke-free workplace policies are the only effective approach to ensure that SHS exposure does not occur in the workplace (1). Separating smokers from nonsmokers, + cleaning the air, and ventilating buildings cannot eliminate SHS exposure (1). Smoke-free laws and policies reduce SHS exposure and improve health among nonsmoking restaurant and bar employees, and reduce SHS exposure among nonsmokers in general, as assessed by self-report and objective measures (1,6–8). Smoke-free workplace policies also help smokers quit (1). Smoke-free policies do not have an adverse economic effect on restaurants and bars (1). Studies also have reported high levels of public support for and compliance with smoke-free laws (1).

The findings in this report are subject to at least three limitations. First, the STATE System captures only certain types of state smoking restrictions (primarily statutory laws and executive orders) and does not capture state administrative laws, regulations, or implementation guidelines. As a result, the manner in which a state smoking restriction is implemented in practice might differ from how it is coded in the STATE System. Second, some state smoking restrictions apply only to private-sector worksites with more than a specified number of employees, to restaurants with more than a specified number of seats, or to bars of at least a certain size. In these cases, the state laws were coded according to the level of these restrictions, even though these restrictions do not apply to venues that are below the specified limits. Finally, because the STATE System only collects state-level data, it does not reflect local smoking restrictions in effect in many states.

The 2006 Surgeon General's Report on The Health Consequences of Involuntary Exposure to Tobacco Smoke concluded that SHS causes premature death and disease in children and nonsmoking adults (1). The report also concluded that no level of SHS exposure is risk free and that only completely smoke-free environments fully protect nonsmokers from SHS exposure (1). States, communities, employers, business proprietors, and the public are acting on this information to reduce SHS exposure. The American Nonsmokers' Rights Foundation estimates that, as of April 2008, 33% of U.S. residents have been living under state or local laws that make worksites, restaurants, and bars completely smoke-free, and 64% of U.S. residents have

*The Guide to Community Preventive Services also reported strong evidence that smoke-free policies reduce SHS exposure. Task Force on Community Preventive Services. The guide to community preventive services: what works to promote health? New York, New York: Oxford University Press, 2005. Available at http://www.thecommunityguide.org/tobacco/tobacco.pdf.

been living under state or local laws making at least one these three settings smoke-free (9). Largely because of the trend toward increased protection by state and local smokfree laws and voluntary policies covering worksites and public places, SHS exposure among U.S. nonsmokers has decreased substantially since 1988 (10). The trends in the adoption of state smoking restrictions described in this report suggest that the national health objective of establishing laws making indoor public places and worksites smoke-free in all states by the year 2010 might be achievable.

Acknowledgments

This report is based, in part, on contributions by C Baker, SS Eidson JD, R Patrick, JD, MayaTech Corporation, Silver Spring, Maryland J Chriqui, PhD, Univ of Illinois at Chicago; J O'Connor, JD, Emor Univ, Atlanta, Georgia; G Vaughn, D Shelton, MPH, A Trosclair, MS Office on Smoking and Health, and NA Blair, MPH, Div of Heart Disease and Stroke Prevention, National Center for Chronic Disease Prevention and Health Promotion, CDC.

References

1. US Department of Health and Human Services. The health conse quences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, GA: US Department of Health and Human Services, CDC, 2006. Available at http://www.surgeongeneral.go library/secondhandsmoke/report.

2. US Department of Health and Human Services. Healthy people 2017 midcourse review. Washington, DC: US Department of Health and Human Services; 2006. Available at http://www.healthypeople.go data/midcourse.

3. CDC. State smoking restrictions for private-sector worksites, restaurants and bars-United States, 1998 and 2004. MMWR 2005;54:649–53. 4. CDC. State Tobacco Activities Tracking and Evaluation (STATE) S tem. Atlanta, GA: US Department of Health and Human Service CDC; 2008. Available at http://www.cdc.gov/tobacco/statesystem. 5. US Department of Commerce, Census Bureau. National Cancer Inst tute and CDC co-sponsored tobacco use special cessation suppleme to the current population survey, 2003 (TUSCS-CPS). Washingto DC: US Department of Commerce, Census Bureau; 2006. Available a http://riskfactor.cancer.gov/studies/tus-cps.

6. Menzies D, Nair A, Williamson PA, et al. Respiratory symptom pulmonary function, and markers of inflammation among bar worke before and after a legislative ban on smoking in public places. JAM 2006;296:1742-8.

7. Goodman P, Agnew M, McCaffrey M, Paul G, Clancy L. Effects of t Irish smoking ban on respiratory health of bar workers and air qualit in Dublin pubs. Am J Respir Crit Care Med 2007;175:840–5.

8. CDC. Reduced secondhand smoke exposure after implementation a comprehensive statewide smoking ban - New York, June 26, 20 June 30, 2004. MMWR 2007;56:705-8.

9. American Nonsmokers' Rights Foundation. Summary of 100 smokefree state laws and population protected by state and local law Berkley, CA: American Nonsmokers' Rights Foundation; 2008. Ava able at http://www.no-smoke.org/pdf/summaryuspoplist.pdf.

10. Pirkle JL, Bernert JT, Caudill SP, Sosnoff CS, Pechacek TF. Trends the exposure of nonsmokers in the U.S. population to secondha smoke: 1988-2002. Environ Health Perspect 2006;114:853–8.

Enteroviruses generally cause mild disease; however, neotes are at higher risk for severe illness because of the maturity of their immune systems. Neonatal systemic terovirus disease, characterized by multiorgan involveent, is among the most serious, potentially fatal condions associated with enterovirus infection. Typical clinical esentations include encephalomyocarditis (characteristic group B coxsackieviruses) and hemorrhage-hepatitis synome (typical of echovirus 11) (1,2). To describe the verity of neonatal illness associated with coxsackievirus 1 (CVB1) infection, CDC analyzed case reports and preninary data from the National Enterovirus Surveillance stem (NESS) for 2007. This report describes the results that analysis, which indicated that, in 2007, CVB1 for e first time was the predominant enterovirus in the United ates, accounting for 113 (25%) of 444 enterovirus infecons with known serotypes. In addition, phylogenetic alysis of the 2007 CVB1 strains suggested that the cases sulted from widespread circulation of a single genetic linge. Health-care providers and public health departments ould be vigilant to the possibility of neonatal disease used by CVB1. Testing for enteroviruses in clinically comtible cases and reporting of identified enteroviruses to ESS should be encouraged.

NESS is a voluntary, passive surveillance system for moniring enterovirus infections in the United States. Particiting laboratories, which include public health and private Doratories and the CDC Picornavirus Laboratory, report terovirus detections to NESS on a monthly basis. Each port includes age, sex, state, specimen type and collecon date, and enterovirus serotype. Beginning in August 2007, CDC received multiple orts of cases of severe neonatal illness and death associd with enterovirus infection. CVB1 was identified as the usative agent in many of these cases. Previously, no fatal ection of CVB1 had been reported to NESS (3). On the sis of these reports, CDC began a review of clinical, viroic, and surveillance data related to enterovirus for 2007, collaboration with local and state public health departnts and hospitals. A case of CVB1 infection was defined detection of enterovirus by reverse transcriptionlymerase chain reaction (RT-PCR) or viral culture, with virus typed as CVB1 by molecular (i.e., RT-PCR uencing) or antigenic (i.e., neutralization or immunof rescence) methods.

As of February 1, 2008, NESS had received 514 reports of enterovirus infections in 36 states for 2007. CVB1 was the most commonly detected enterovirus reported to NESS, accounting for 113 (25%) of 444 reports with known serotypes (Figure). Other most frequently reported serotypes included echovirus 18 (63 [14%]), echovirus 9 (49 [11%]), and echovirus 6 (37 [8%]). Children aged <1 year accounted for 65 (68%) of 95 CVB1 reports with known age, including 50 (53%) infants aged <1 month. CVB1 was detected in 19 states; 58% of all CVB1 detections were reported from California (n = 38) and Illinois (n = 28). Phylogenetic analysis of current CVB1 strains based on partial sequence of the VP1 gene revealed that all were closely related to each other and to a 2006 strain from Colorado. Analysis also revealed that the strains were more distantly related to earlier strains.

A total of five CVB1-associated neonatal deaths were identified: two from California, one from Illinois, and one death each from Colorado and New Mexico. These came to CDC attention in connection with requests for laboratory assistance (Table). In all five cases, the neonates had multisystem disease with onset within the first 4 days of life. In four of the five fatal cases, the mothers had febrile illness or chorioamnionitis around the time of delivery, suggesting vertical mother-to-infant transmission.

The three distinct clusters of severe enterovirus illness, including illnesses caused by CVB1, detected in Los Angeles, California, Chicago, Illinois, and Kotzebue, Alaska, during 2007 are described below.

Los Angeles County, California. In September 2007, in response to reports of three cases (two of them fatal) of neonatal enterovirus myocarditis, including two in CVB1positive neonates, the Los Angeles County Department of Public Health asked all hospitals in the county to report

1

State

California

all enterovirus-positive cases of severe or fatal myocarditis, aseptic meningitis, or sepsis-like febrile illness that occurred among children during June-November 2007.

A total of 30 enterovirus-positive patients from seven hospitals were identified (all with illness diagnosed by RTPCR). Median age was 15 days (range: <1 day-14 years); 22 (73%) were aged <1 month. Four (13%) patients aged <1-7 days died, and another 14 (47%) required intensivecare unit (ICU) treatment. Clinical presentations included meningitis (22 patients), myocarditis (12), sepsis-like illness (five), hepatitis (two), coagulopathy (six), and respiratory difficulties (three). Eleven patients, including all nine patients aged <7 days at admission, had illness with multiorgan involvement.

Enterovirus serotype was determined in 19 cases for which isolates obtained by viral culture were available. CVB1 accounted for 14 cases; CVB2 accounted for two cases, and CVB3, CVB4, and echoviruses 7 and 11 accounted for one case each. One patient was coinfected with CVB1 and CVB3. Two of the four patients who died were infected with CVB1 (Table). Specimens from the other two patients who died were not available for virus characterization.

Chicago, Illinois. In September 2007, the CDC Picornavirus Laboratory identified CVB1 as the source of

Virus detection CVB1 isolated from blood

CVB1 isolated from cerebrospina fluid (CSF)

CVB1 detected by reverse transcription-polymerase chain reaction (RT-PCR) in CSF and isolated postmortem from heart tissue

CVB1 detected by RT-PCR in CSF and in serum

CVB1 isolated premortem from nasopharyngeal and rectal swabs and isolated postmortem from lungs and nasopharyngeal swab

infection in two cases of severe neonatal disease at Children's Memorial Hospital in Chicago. Subsequently, a review of the hospital's laboratory and medical records was conducted to identify additional enterovirus-positive cases and obtain diagnoses and clinical syndrome information. Fifty enterovirus-positive children (all diagnosed by RT-PCR) were admitted during June 6-November 2, 2007, a two-fold increase compared with the entire years 2005 (25 patients and 2006 (26 patients). Median age of patients was days (range: <1 day-8 years); 40 (80%) patients were aged ≤1 month.

Serotype was determined for nine patients admitted to ICU; CVB1 was found in eight patients, and echovirus 18 in one patient. In two other patients, an enterovirus was identified by immunofluorescence staining as a group coxsackievirus. Specimens from the remaining 39 RT-PCRpositive patients were not available for further virus characterization.

Twelve (24%) infants aged <1-12 days required ICU admission. Their clinical presentations included myocard.c (11 patients), respiratory distress (nine), hepatitis (eight. coagulopathy (six patients), aseptic meningitis (four), and meningoencephalitis (three). Eleven (92%) patients had multiorgan involvement, including five with myocarditis

Geningitis, or meningoencephalitis, and hepatitis (three so had coagulopathy). One CVB1-positive patient died Table), and one required heart transplantation. Kotzebue, Alaska. In early September 2007, Maniilaq ealth Center notified the Alaska Department of Health id Social Services of an increase in severe febrile illness nong hospitalized young infants (including three with yocarditis). Medical record review indicated that during ugust 15-September 11, 2007, seven infants aged I month (23% of 31 babies born in the Northwest Arctic orough region since July 1, 2007) had been admitted to e health center with fever and respiratory distress, myorditis, or meningitis (median age: 18 days; range: 5-48 ys). Six patients, five with multiorgan involvement, quired ICU treatment, referral to a higher-level hospital, both. Of these, three patients had myocarditis with asepmeningitis and respiratory failure (including one with evated liver enzymes and coagulopathy), two had aseptic eningitis and respiratory distress, and one had aseptic eningitis. The patient with milder illness had a febrile ndrome. None of the patients died.

One patient with myocarditis tested enterovirus-positive RT-PCR, but the specimen was not available for further us characterization. CVB1 was isolated from a stool specien of the patient with aseptic meningitis. The etiologic ent remained unknown in five cases. In addition, CVB1 is isolated from a respiratory specimen of an infant aged months with pneumonia who was treated at the health nter as an outpatient during the same period.

ported by: L Mascola, MD, D Terashita, MD, Acute Communicable sease Control, Los Angeles County Dept of Public Health; MB Salzman, D, Kaiser Permanente West Los Angeles Medical Center; D Schnurr, PhD, agi, T Padilla, Viral and Rickettsial Disease Laboratory, California pt of Public Health. N Verma, MD, XZheng, MD, PhD, ST Shulman, D, Children's Memorial Hospital, Northwestern Univ Feinberg School Medicine; MU Harris, MSN, Children's Memorial Hospital, Chicago, nois. R Gibson, MD, Maniilaq Health Center, Kotzebue; E Funk, MD, iska Dept of Health and Social Svcs; T Schmidt, MS, M Westcott, Alaska te Virology Laboratory. C Robinson, PhD, Children's Hospital, Aurora, lorado. JP Burns, MD, JD, Dept of Pathology, Univ of New Mexico ool of Medicine, Albuquerque; Scientific Laboratory Div, New Mexico bt of Health. N Khetsuriani, MD, PhD, SOberste, PhD, M Pallansch, D, A Fowlkes, MPH, M Wikswo, MPH, Div of Viral Diseases, National nter for Immunization and Respiratory Diseases; Div of Viral and kettsial Diseases, National Center for Zoonotic, Vector-Borne and Enteric eases; K Sircar, EIS Officer, CDC.

itorial Note: In 2007, an increased level of CVB1 activwas associated with severe neonatal disease and mulle deaths in the United States. The actual extent of 'B1-associated morbidity and mortality likely was much ater because 1) nonpolio enterovirus infections are not ionally reportable, 2) diagnostic testing for enteroviruses

often is not pursued in clinical settings, and 3) serotype identification from enterovirus-positive specimens is not performed routinely. CVB1 has an epidemic pattern of circulation, with increases usually lasting 2-3 years (Figure). During 1970-2005, CVB1 accounted for a small (2.3%) but increasing proportion of all enteroviruses reported in the United States (3). In 2007, CVB1 was the most commonly reported serotype, accounting for 25% of all reported enterovirus infections with known serotypes. Until 2007, CVB1 had never been the most commonly reported serotype and, even in peak years, accounted for <10% of all enterovirus reports (Figure). The year 2007 also was unusual for the number of CVB1-associated fatalities reported to NESS: 5 fatal cases were reported for the year. CVB1associated deaths are reported rarely (4–6), and had not been reported previously to NESS (3,7).

Historically, two thirds of CVB1 detections have been among children aged <1 year (3). During 1983-2003, neonates accounted for 22% of CVB1 reports versus 11% for other enteroviruses (7), suggesting a propensity to infect newborns. Cases of neonatal CVB1-associated disease identified in 2007 were characterized not only by myocarditis and central nervous system involvement typical of group B coxsackieviruses but also, on multiple occasions, by hepatitis and coagulopathy, which usually are reported with echovirus 11 infections.

Enterovirus infections are common, particularly during summer-fall months and typically are spread person-toperson via the fecal-oral or oral-oral routes and through respiratory droplets and fomites. Perinatal transmission from mother to infant occurs transplacentally or from exposure to maternal blood or secretions during delivery. Maternal enterovirus illness around the time of delivery and lack of maternal antibodies to an infecting serotype increase the risk for transmission. Onset of enterovirus disease resulting from perinatal transmission occurs in the first 1-2 weeks of life and carries a higher risk for severe illness and death than enterovirus infection acquired during the postnatal period (1,2,8).

No treatments approved by the Food and Drug Administration for enterovirus are available. Intravenous immunoglobulin sometimes is used, but its effectiveness in neonatal enterovirus disease is uncertain (2). Use of the candidate antiviral drug pleconaril (Schering-Plough, Kenilworth, New Jersey) showed benefit in neonates with life-threatening enterovirus disease (9); a phase 2 clinical trial of pleconaril in neonates is under way (10).

In the absence of vaccines, nonpolio enterovirus transmission can be reduced by adherence to good hygienic practices, such as thorough hand-washing (especially after