Introduction to implied volatility surfaces

Maternal exposure to arsenic has been observed to occur from due to workplace

exposure, smoking. diet, and through exposure to contaminated drinking \\'liter, house

dust, and ambient air (Tnbncova, 1986). In exposed mothers, As is said to be present in maternal blood, readily crosses the foeto-matemnl interface and accumulates in certain

foetal tissues including the placenta at concentrations much greater than that in maternal blood (Shnlat ct al 1996). Foetal blood As levels ore believed to increase ,,ith gestational time (Lugo et al, 1,969). I lo,,cvcr, DeScsso ( 1998) postulated that under environmentally relevant exposure scenarios (e.g. I OOppm in soil), inorganic arsenic is unlikely to pose: a risk to pregnant \\On1en .ind their offspring.

The reproductive toxicity of acute ^1\!> exposure has been established. ,,·hilc that of prolonged lo,v-lcvel exposure is yet to be adequately defined. Current opinion among researchers, regulatory agencies and other orgoni,.ations is ofien contradictory.

In a 1991 publication the non-rcgulntory ,\gcncy for Toxic Substnnccs and Disease Registl') (L'SPIIS ATSDR), b:.1sing risk ,1sscssn1cn1 prin1aril) on hun1on metabolic studies and chn1cal case�. found As to be potentinll ⁾ foeto-toxic and teratogenic onl ⁾ at doses hkel ⁾ to cau.,e maternal toxicit). \\ 11ilc some unccna1ntics 1n the n:productivc bl:ha, iour or As exist, science has pro, cd that ,\s is indeed a corcinogcn. potential humon tcratogcn, and possihlc cause or hun1nn Nms, f'unhcr rcsc:Mch into the toxicll) and 1ero1ogcn1ci1� of As ,vould conllnue 10 be ncccssan _• cspcciall) in the areas or 1nvcs11gouon of the specific mechanism of nrscnic-nssociotcd

teratogenesis and nil its po1cn1iol reproductive outcomes. It 1s being suggested ho\\c:\ er

that the metalloid is considered a probable hum11n rcproducth c toxin

proteins (hsps) and specifically results in N ros in laboratory animals (�1irkes et al (1992).

Further more, prenatal exposure synergistically increases the incidence of NTDs follo""ing nu1temal hypenhermin (nnd hos been linked \\ilh the occurrence of decreased foetal ,veight in exposed groups (Craig el al. ( 1995). Thus confirming the result of an

earlier study published by Nordstrom and co-,vorkcrs ( 19780) in ,vhich "'on1cn employed at the Ronnskar facility and those living ,, ithin IO ^km of the plant 10 S,vcden gave binh to children \\'ith lo,ver birth \\eights than lhose in the control group. This decrease ,vns found to bl! pronounced 1n Inter pregn ^an cies (Nordstrom, ct al, 1978a). In

a similar study carried out the same year, Nordstrom et al ( 1978b), examined retrospective!) the frequency of spontaneous abortion occurring in the population living around the Ronnskor smelter exposed as a result of proximity of the "·omen's homes to the plant. It ^\\'llS found that \\omen living close to the plant cxpcncnct!d rates of spontaneous abortion that \\ere significantly greater thon those farther ^O\\O) from the plant. In addition to this. ,,;omen living closest to the plant ,vere observed to have higher proportion of adverse: pregnancy outcomes (Nordstrom ct nl 19790). The problem ^\\'OS observed to be more pronounced ,vhcn the father ,vos also employed in the pl ^an t. J"hc

conclusion dra\\11 from I.he study "'as thut the observed mnlformntion ,.,.'llS ^{due 10 d 11 �c1}

1cratogcn1c1t) of toxin exposures ut the plant •

.\ further :.tud) by the authors (Nordstrom e1 nl, 1979b), considcrct.l uni} the employees of the plant in order to deicrmine exposure status Results indicated that ofl :.pnngs of female employees exhibited increased rotes of congcnllul mulformations and

a study carried out by Beckman ( 1978) on foc:tol ntortaht) a1nonK ,vives of nten employed 111 the Ronnskar smelter obsm cd that the rate:, ol stillbinh (foet:il mortlllil)·)

\\ere significant!) higher nmong the exposed \\'Orkcrs 1h1111 n,nong non.cxpo�1.-d

\\'Orl.crs. It ^\\OS therefore sugge$lcd that thi, cflcct could not hu\c bt:cn due to an alteration of the sperm but could be Jue to exposure of \\orl.:cri;' \\hes due to dust conlllmiruuon on ^\\01kcrs' clothes llcsults ot vnnous cp ¹ d1:n11ulog ¹ cal filudics nntl rcvic\\-s on the rcproJuctl\c toxiCII) of nrscn11: hn,e suggested thnt 1n nemal c posurc to the mct,:l1l01d mn) �rt1cul11rl) explo1n ntnn) unnccoun111ble cnrl> 1nb�.1rr ¹ ngc� (�h ^:i l ^;t t, ct ul, 1996)

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2. 14. Arsenic as a tcratogcn

For decades, arsenic has been recognized as a 1erotogen resulling from ou1con1c of studies ,vhich demonstrated the development of a variety of molformations follo\\'1ng lo,v-levct arsenate exposure in chick ernb _ry os (Ancel et ol. 1941 ). Recent studies ha,e further reinforced this cloim. Gilani cl al ( 1990) documented in vitro en,ironn1en1 increased incidence of everted viscer� microphhthalmia ^an d emb _ry onic deoth resulting from exposure to arsenic. Shala1 ( 1996) referred to consistent findings of over thirt)

studies particulorly in rodents conlim1ing si1nilar results. Clcll palate and skeletal, ophthalmic and uro-genital malformations have been invariably induced in rodents '"hile foetal gro,vth retardation as ,veil as emb _ry onic deaths is general! _.> increased

folto"'·ing prenatal exposure to arsenic. Abnormal neurological development in neonate mice prenatally exposed to lo,\ dosc:s of arsenic hos also been reported (�fa el al, ^1994).

The priority accorded research on inorganic arsenic 1ox1c1ty on one h ^an d, the discussions of lhe effects on developing vertebrates 1n vnriol!li compendia (Shepard,

1995). nnd the extent and conclusions of several rcvic,vc:d papers on the subJect hove led the fcdc:rol and state agencies in the USA to 1dentif .> Arsenic as o cnndidotc for assessment of reproductive and/or dcvclopn1en1at toxicny (DeScsso ct al, t ⁹⁹⁸⁾ In general the orgo.nie form of the metalloid is nol considered to be toxic und has been of

less concern \Vith regard to S)stemic toxicity (Vnhtcr, 1994 ⁰ ).

2. I 5. Ar�cnic :ind its u-.c 11s Pc.sticidcs

The uses of nrscn1c 1n the prudu,uon of o ,,·idc: rungc or pesticides as \\ell ns defoliant in cotton lutrvest111g have been \vich�I> reported (Shnln1 ct 111 1996) �Ian)

hul1\i.lll studies h.a\c reported incrcasc-d mtcs of NI Os in assoc1a11on \\ith c,posurc to pesticides (Bahuajan cl nl, 1983: \\'l111c ct 111, 1988· Urcndcr ct al, 1990), In n stud> of so,nc con1n1unnic:s near llunford 111 USA, elc�,llcd ^r-,11.:s ol l\'Tl>s \\ere ohscT\cd ( 17 2 per 10,000 birth�) o, er ^II period of 12 years 1n o cohort stud)' of 23,000 h ¹ rths l \\'llltc ^Cl

111. 191!8). TI ¹ c wiJcsprc&J ^USC of pesticides In the co111n1unit1cs 1n11Jc the nuthoT!i lo suggcsl further studies into the u�u111on bcl\\ttn NI Us nnJ the chcrn ¹ cnl,, "nother t.tud) in Cannd:i cumcd out spccitlcnll) to look ^filr nssoclallon bc1,,ccn h ⁱ rth dcfccl!,

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and agricuhural exposures (\Vhitc el al. 1988) reported a statistical!} significant doubling of the number of cases of congenital malfom1ations including ancnccphaly.

spinal bifida, clef\ palate. cleft lip and renal ugencsis.

Similar studies in l:ngland on association bcl\vecn birth dcft:cts and occupation in agriculture (Balarojan cl al, 1983) indicated o modest increased risk of similar conditions among off springs of gardeners and grounds men but not otht:r agricullurol occupations. thus c�tablishing the culpabilit) of pesticides. ,\nolht:r stud) conductt:d among sol\'enl-cxposcd \\Orkers in Texns (Brender ond Suarez, 1990) reported a 28 ^° 0 increase in the risk ofNTDs in o!Tspring of pcs1 ¹ c1dcs-cxposcd ,,orkcrs und un increase of 73°/o in those of filnn and ranch \\orkcrs. although neither of these findings ,vas

:.tat1s11call _} si _gn ificant. I lowcvcr, in a case control stud) carru:d out 10 e\'aluotc o cluster ofN"I Os ¹ n Oro,\nsvillc, Tt:xos ( 1 l)oll. 1992). a s1a11s11call) sigrulicant incrt:asc

of 330�:i for NTDs ^\\'tlS reported to be associated ,vilh aerial spm)'ing of pcs1ic1des on crops.

Several ca�es of ,\s poisoning has been n:ported fron1 paris-gn:cn (copper aeelO·

ursenite) factories 10 Calcutt.1, Ind ⁱ o (uuha et al I 992), n1incs in 1 oruku and NakoJo.

Jnpan (I sudo, ct al, 1989: Tsudu ct al. 1990; I sudu ct ul. 1995) ond Reichcns1c ¹ n, Poland (Sch\\tll'U., 1993) and few ^{t:lSCS 1} n �lolays,a (Ja.1far et al I Q93). Exposure to ,n�cctic ¹ des and pa11c ¹ dcs 1n \\1nc: moking 1111d \\Ork,ny \\1th \\OOd hll.5 been said 10 ha\c the possibilit) of rcsul11ng 1n10 chronic poi\on,ng ( l sudo ct al I 9QS) Dich ct nJ ( t 997) asserted 1hn1 1n human.�. an;c:n1c cornpounds und insccucidcs used occup:111oruill)

have been cla��ilicJ ^o., curc ¹ no�c1uc b) the lnlcmauonal ,\1&cncy tor Resenn:h on Cancer (lAltC). lluman datu ore ho,,c\cr lim11ed by the small nu111hcr of studies th:it

c, uhmlc 1nJ ¹ \ uluJI pc$llt1dcs und 1l11� ha� been 1dcnt1hcd a rcsc,irch pnont) orcn

\\'b ⁱ le 5,0n1c 1nform1111on 1s n,n,lnhlc un the spcc ¹ 1ic pc 11cidcs, in general most epidcmiolo&JC studies h11, c little specific qu11lim1ivc let alone qu11111iln1h c: dntll on the specific pcJ.llcidc exposure llo,,c,cr g ¹ ,cn the ,,,desprcnJ hiMoru.:al use ol nrscn,cols ,n ognculturc and 11s pcrs1�1cncc u, the tnv1ronn1cn1, 1hc poss1h ¹ llt) thn1 the ob�f\'Cd

,ncrc:iscd nsk of N'J 1)5 1n oiv•�uhunil popul1111ons ma} he 011nbu1nblc to ftrscn,c should be cnrcfully cons1Jcrcd (Shnlo1, cl nl, 1996)

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